Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_896_Библиотеки_им_академика_М_И_Перельмана
.pdf
316
https://t.me/med1917
R. Roy et al.
Fig. 17.1 Immune dysregulations and dysfunctions in diabetic wounds
during the acute phase of healing. (1) In the early phase of wound healing following an injury, diabetic wounds have a lower number of phagocytic leukocytes (PMNs and Møs) due to dysregulation in cell adhesion
molecules, reduced expression of FPR and CXCR2 chemokines. These
wounds also exhibit elevated levels of IL-10. (2) The low numbers of
PMNs and Møs and high IL-10 levels in diabetic wounds result in
TLRs. Consequently, there is a reduction in proinammatory
cytokine expression, which further contributes to the
decreased number of PMNs and Møs in these wounds. The
lower numbers of PMNs and Møs in diabetic wounds, along
with their impaired antimicrobial functions, make diabetic
wounds more susceptible to infection by pathogenic bacteria
such as S. aureus and P. aeruginosa.
As bacteria establish infection in diabetic wound, they
produce virulence factors (cytotoxins and immune regulators), and biolm (in majority of cases) that further protect
them from innate immune system defenses. Over time, the
accumulation of biolms and bacterial products known as
pathogen-associated molecular pattern molecules (PAMPs)
leads to the activation of innate immune responses through
pattern recognition receptors (PRRs) such as TLRs.
Activation of TLRs results in the production of more proinammatory cytokines, which attract and accumulate additional inammatory leukocytes, such as PMNs and Møs to
the wound site. As a result of this inux of immune cells,
PMNs and inammatory Møs (M1) produce higher levels of
proinammatory cytokines and proteases, including NE and
MMPs. These enzymes can then break down growth factors
and the extracellular matrix, which further sustain inamma-
reduced expression and signaling through TLRs. (3) As a consequence,
there is a decrease in the expression of proinammatory cytokines,
which further contributes to the reduced numbers of PMNs and Møs in
these wounds. (4) The reduced numbers of PMNs and Møs in diabetic
wounds, coupled with their impaired antimicrobial functions (5), make
diabetic wound susceptible to infection by pathogenic bacteria such as
S. aureus and P. aeruginosa
tory environment, driving diabetic wounds toward chronic
non-healing state and possibly amputation, thus accounting
for the deleterious impact of pathogenic bacteria on wound
healing outcomes in DFUs (Fig.17.2).
To conclude this chapter, we discussed various approaches
to managing infections in diabetic wounds, encompassing
conventional, unconventional, and emerging treatment methods. Conventional treatments for diabetic foot ulcers (DFUs)
involve debridement, ofoading, wound dressing, antibiotics, and glycemic control (Table17.4). Unconventional treatments for DFUs include silver, honey, hyperbaric oxygen
therapy (HBOT), and maggot debridement therapy (MDT)
(Table17.5). Emerging therapies consist of AMPs-, bacteriophage-, and immunomodulator-based treatments
(Table 17.6). It is important to highlight that maintaining
proper glycemic control continues to be one of the most
effective approaches for preventing infections in diabetes,
considering the multiple negative effects that elevated glucose levels have on immune system function.
Acknowledgments This work was supported by the National Institutes
of Health (NIH) grants RO1DK107713, R01AI150668, R01DK135557,
and R21AI110685 (All to S.H.S.).
17 Infection inDiabetes: Epidemiology, Immune Dysfunctions, andTherapeutics
https://t.me/med1917
317
Fig. 17.2 Infection as a major driver of non-healing chronic ulcers in
diabetic wounds. (1) In diabetic wounds, bacteria often form biolms
upon infection and produce virulence factors that help them evade the
innate immune system’s defenses. (2) Over time, the accumulation of
biolms and bacterial products known as PAMPs leads to the activation
of innate immune responses through TLRs. (3) Activation of TLRs
results in the production of more proinammatory cytokines, which
References
1. Ozougwu J, Obimba K, Belonwu C, Unakalamba C.The pathogenesis and pathophysiology of type 1 and type 2 diabetes mellitus. J Physiol Pathophysiol. 2013;4(4):46–57.
2. Njølstad PR, Sagen JV, Bjørkhaug L, Odili S, Shehadeh N,
Bakry D, Sarici SU, Alpay F, Molnes J, Molven A.Permanent
neonatal diabetes caused by glucokinase deciency: inborn
error of the glucose- insulin signaling pathway. Diabetes.
2003;52(11):2854–60.
3. Gregg EW, Sattar N, Ali MK.The changing face of diabetes complications. Lancet Diabet Endocrinol. 2016;4(6):537–47.
4. Harding JL, Pavkov ME, Magliano DJ, Shaw JE, Gregg
EW.Global trends in diabetes complications: a review of current
evidence. Diabetologia. 2019;62(1):3–16.
5. Vigneri P, Frasca F, Sciacca L, Pandini G, Vigneri R.Diabetes and
cancer. Endocr Relat Cancer. 2009;16(4):1103–23.
6. Ducat L, Philipson LH, Anderson BJ.The mental health comorbidities of diabetes. JAMA. 2014;312(7):691–2.
7. Nagendra, L., H.Boro, and V.Mannar, Bacterial infections in diabetes. Endotext [Internet]. 2022.
8. Lao M, Li C, Li J, Chen D, Ding M, Gong Y.Opportunistic invasive fungal disease in patients with type 2 diabetes mellitus from
Southern China: clinical features and associated factors. J Diabet
Investig. 2020;11(3):731–44.
9. Rodrigues CF, Rodrigues ME, Henriques M. Candida sp. infections in patients with diabetes mellitus. J Clin Med. 2019;8(1):76.
10. Klekotka RB, Mizgała E, Król W.The etiology of lower respiratory tract infections in people with diabetes. Adv Respir Med.
2015;83(5):401–8.
attract and accumulate additional inammatory leukocytes, such as
PMNs and Møs to the wound site (4). (5) As a result of this inux of
immune cells, PMNs and inammatory Møs (M1) produce higher levels of proinammatory cytokines and proteases, including NE and
MMPs. These enzymes can then break down growth factors and the
extracellular matrix, leading to chronic non-healing wounds and possibly amputation (6)
11. Op de Beeck A, Eizirik DL.Viral infections in type 1 diabetes mellitus—why the β cells? Nat Rev Endocrinol. 2016;12(5):263–73.
12. Zhang X, Zhu X, Ji Y, Li H, Hou F, Xiao C, Yuan P.Increased risk
of hepatitis B virus infection amongst individuals with diabetes
mellitus. Biosci Rep. 2019;39(3):BSR20181715.
13. Malhotra R, Chan CS-Y, Nather A.Osteomyelitis in the diabetic
foot. Diabet Foot Ankle. 2014;5(1):24445.
14. Rodríguez-Rodríguez N, Martínez-Jiménez I, García-Ojalvo A,
Mendoza-Mari Y, Guillén-Nieto G, Armstrong DG, BerlangaAcosta J.Wound chronicity, impaired immunity and infection in
diabetic patients. MEDICC Rev. 2022;24:44–58.
15. Acosta JB, Garcia del Barco D, Cibrian Vera D, Savigne W, LopezSaura P, Guillen Nieto G, Schultz GS. The pro- inammatory
environment in recalcitrant diabetic foot wounds. Int Wound J.
2008;5(4):530–9.
16. Pouget C, Dunyach-Remy C, Pantel A, Schuldiner S, Sotto A,
Lavigne J-P. Biolms in diabetic foot ulcers: signicance and
clinical relevance. Microorganisms. 2020;8(10):1580.
17. Metcalf DG, Bowler PG.Biolm delays wound healing: a review
of the evidence. Burns Trauma. 2013;1(1):5–12.
18. Boulton AJ, Armstrong DG, Hardman MJ, Malone M, Embil
JM, Attinger CE, Lipsky BA, Aragón-Sánchez J, Li HK, Schultz
G. Diagnosis and management of diabetic foot infections.
Compendia. 2020;2020(1):1.
19. Kim EJ, Ha KH, Kim DJ, Choi YH.Diabetes and the risk of infection: a national cohort study. Diabetes Metab J. 2019;43(6):804.
20. Carey IM, Critchley JA, DeWilde S, Harris T, Hosking FJ, Cook
DG.Risk of infection in type 1 and type 2 diabetes compared with
the general population: a matched cohort study. Diabetes Care.
2018;41(3):513–21.
318
https://t.me/med1917
R. Roy et al.
21. Phillips JS, Jones SE. Hyperbaric oxygen as an adjuvant treatment for malignant otitis externa. Cochrane Database Syst Rev.
2013;5:CD004617.
22. Nitzan O, Elias M, Chazan B, Saliba W.Urinary tract infections in
patients with type 2 diabetes mellitus: review of prevalence, diagnosis, and management. Diabetes Metab Syndr Obes. 2015;8:129.
23. Jay CA, Solbrig MV.Neurologic infections in diabetes mellitus.
Handb Clin Neurol. 2014;126:175–94.
24. Pearson JA, Tai N, Ekanayake-Alper DK, Peng J, Hu Y, Hager
K, Compton S, Wong FS, Smith PC, Wen L.Norovirus changes
susceptibility to type 1 diabetes by altering intestinal microbiota
and immune cell functions. Front Immunol. 2019;10:2654.
25. White D, Ratziu V, El-Serag H. Hepatitis C virus infection and
type 1 and type 2 diabetes mellitus. J Hepatol. 2008;49:831–44.
26. Knobler H, Schihmanter R, Zifroni A, Fenakel G, Schattner
A.Increased risk of type 2 diabetes in noncirrhotic patients with
chronic hepatitis C virus infection. In: Mayo Clinic proceedings,
vol. 75. Elsevier; 2000. p.355.
27. Mangia A, Schiavone G, Lezzi G, Marmo R, Bruno F, Villani
MR, Cascavilla I, Fantasia L, Andriulli A.HCV and diabetes mellitus: evidence for a negative association. Am J Gastroenterol.
1998;93(12):2363–7.
28. Šestan M, Marinović S, Kavazović I, Cekinović Đ, Wueest
S, Wensveen TT, Brizić I, Jonjić S, Konrad D, Wensveen
FM.Virus-induced interferon-γ causes insulin resistance in skeletal muscle and derails glycemic control in obesity. Immunity.
2018;49(1):164–177.e6.
29. Mair M, Singhavi H, Pai A, Singhavi J, Gandhi P, Conboy P, Baker
A, Das S.A meta-analysis of 67 studies with presenting symptoms and laboratory tests of COVID-19 patients. Laryngoscope.
2021;131(6):1254–65.
30. Maharaj S, Ahmed S, Pillay P.Deep neck space infections: a case
series and review of the literature. Clin Med Insights Ear Nose
Throat. 2019;12:1179550619871274.
31. Adegbiji WA, Aremu SK, Olatoke F, Olajuyin AO, Ogundipe
KO.Epidemiology of otitis externa in developing country. Int J
Recent Sci Res. 2017;8(6):18023–7.
32. González JLT, Suárez LLR, de León JEH.Malignant otitis externa:
an updated review. Am J Otolaryngol. 2021;42(2):102894.
33. Khanna M, Challa S, Kabeil AS, Inyang B, Gondal FJ, Abah
GA, Dhandapani MM, Manne M, Mohammed L.Risk of mucormycosis in diabetes mellitus: a systematic review. Cureus.
2021;13(10):e18827.
34. Reddy SS, Rakesh N, Chauhan P, Sharma S. Rhinocerebral
mucormycosis among diabetic patients: an emerging trend.
Mycopathologia. 2015;180(5):389–96.
35. Kazak E, Aslan E, Akalın H, Saraydaroğlu Ö, Hakyemez B, Erişen
L, Yazıcı B, Gürcüoğlu E, Yılmaz E, Ener B. A mucormycosis
case treated with a combination of caspofungin and amphotericin
B.J Mycol Médicale. 2013;23(3):179–84.
36. Huang T-T, Tseng F-Y, Liu T-C, Hsu C-J, Chen Y-S. Deep neck
infection in diabetic patients: comparison of clinical picture and
outcomes with nondiabetic patients. Otolaryngol Head Neck Surg.
2005;132(6):943–7.
37. Casqueiro J, Casqueiro J, Alves C.Infections in patients with
diabetes mellitus: a review of pathogenesis. Indian J Endocrinol
Metab. 2012;16(Suppl 1):S27.
38. Erener S. Diabetes, infection risk and COVID-19. Mol Metab.
2020;39:101044.
39. Varikasuvu SR, Dutt N, Thangappazham B, Varshney S.Diabetes
and COVID-19: a pooled analysis related to disease severity and
mortality. Prim Care Diabetes. 2021;15(1):24–7.
40. Thomsen WR, Mor A.Diabetes and risk of community-acquired
respiratory tract infections, urinary tract infections, and bacteremia. Open Infect Dis J. 2012;6(1):27.
41. Kornum JB, Thomsen RW, Riis A, Lervang H-H, Schønheyder
HC, Sørensen HT.Type 2 diabetes and pneumonia outcomes: a
population-based cohort study. Diabetes Care. 2007;30(9):2251–7.
42. Kornum JB, Thomsen RW, Riis A, Lervang H-H, Schønheyder
HC, Sørensen HT.Diabetes, glycemic control, and risk of hospitalization with pneumonia: a population-based case-control study.
Diabetes Care. 2008;31(8):1541–5.
43. Banerjee M, Pal R, Dutta S. Risk of incident diabetes postCOVID- 19: a systematic review and meta-analysis. Prim Care
Diabetes. 2022;16:591.
44. Nickel JC, Stephens A, Landis JR, Mullins C, van Bokhoven A,
Lucia MS, Ehrlich GD, MAPP Research Network. Assessment of
the lower urinary tract microbiota during symptom are in women
with urologic chronic pelvic pain syndrome: a MAPP network
study. J Urol. 2016;195(2):356–62.
45. Soh PN, Vidal F, Huyghe E, Gourdy P, Halimi J, Bouhanick
B.Urinary and genital infections in patients with diabetes: how
to diagnose and how to treat. Diabetes Metab. 2016;42(1):16–24.
46. Hirji I, Guo Z, Andersson SW, Hammar N, Gomez-Caminero
A.Incidence of urinary tract infection among patients with type 2
diabetes in the UK General Practice Research Database (GPRD).
J Diabetes Complicat. 2012;26(6):513–6.
47. Kofteridis DP, Papadimitraki E, Mantadakis E, Maraki S,
Papadakis JA, Tzifa G, Samonis G. Effect of diabetes mellitus on the clinical and microbiological features of hospitalized
elderly patients with acute pyelonephritis. J Am Geriatr Soc.
2009;57(11):2125–8.
48. Mnif MF, Kamoun M, Kacem FH, Bouaziz Z, Char N, Mnif F,
Naceur BB, Rekik N, Abid M.Complicated urinary tract infections associated with diabetes mellitus: pathogenesis, diagnosis
and management. Indian J Endocrinol Metab. 2013;17(3):442.
49. Aslonova I, Khazratov UK, Erkinova N, Tosheva H.The prevalence of chronic pyelonephritis in women with disturbed tolerance
for glucose. Asian J Multidimensional Res. 2019;8(11):81–5.
50. Taylor D, Neal D, McBride P.The association between spontaneous pyelonephritis and maturity-onset diabetes mellitus in male
MM mice. Lab Anim. 1987;21(4):318–25.
51. Fünfstück R, Nicolle LE, Hanefeld M, Naber KG. Urinary
tract infection in patients with diabetes mellitus. Clin Nephrol.
2012;77(1):40.
52. Mangram AJ, Horan TC, Pearson ML, Silver LC, Jarvis WR,
Guideline for Prevention of Surgical Site Infection. Centers
for Disease Control and Prevention (CDC) hospital infection
control practices advisory committee. Am J Infect Control.
1999;27(2):97–132; quiz 133–4; discussion 96.
53. Berríos-Torres SI, Umscheid CA, Bratzler DW, Leas B, Stone EC,
Kelz RR, Reinke CE, Morgan S, Solomkin JS, Mazuski JE.Centers
for Disease Control and Prevention guideline for the prevention of
surgical site infection, 2017. JAMA Surg. 2017;152(8):784–91.
54. Allegranzi B, Zayed B, Bischoff P, Kubilay NZ, de Jonge S,
de Vries F, Gomes SM, Gans S, Wallert ED, Wu X, Abbas M,
Boermeester MA, Dellinger EP, Egger M, Gastmeier P, Guirao
X, Ren J, Pittet D, Solomkin JS, W.H.O.G.D.Group. New WHO
recommendations on intraoperative and postoperative measures
for surgical site infection prevention: an evidence-based global
perspective. Lancet Infect Dis. 2016;16(12):e288–303.
55. Martin ET, Kaye KS, Knott C, Nguyen H, Santarossa M, Evans
R, Bertran E, Jaber L. Diabetes and risk of surgical site infection: a systematic review and meta-analysis. Infect Control Hosp
Epidemiol. 2016;37(1):88–99.
56. Kroin JS, Buvanendran A, Li J, Moric M, Im H-J, Tuman KJ,
Shakhani SH. Short-term glycemic control is effective in
reducing surgical site infection in diabetic rats. Anesth Analg.
2015;120(6):1289–96.
57. Kroin JS, Li J, Goldufsky JW, Gupta KH, Moghtaderi M,
Buvanendran A, Shakhani SH. Perioperative high inspired
oxygen fraction therapy reduces surgical site infection
with Pseudomonas aeruginosa in rats. J Med Microbiol.
2016;65(8):738–44.
58. Goldufsky J, Wood SJ, Jayaraman V, Majdobeh O, Chen L, Qin
S, Zhang C, DiPietro LA, Shakhani SH. Pseudomonas aerugi-
17 Infection inDiabetes: Epidemiology, Immune Dysfunctions, andTherapeutics
https://t.me/med1917
319
nosa uses T3SS to inhibit diabetic wound healing. Wound Repair
Regen. 2015;23(4):557–64.
59. Roy R, Zayas J, Singh SK, Delgado K, Wood SJ, Mohamed MF,
Frausto DM, Estupinian R, Giurini EF, Kuzel TM, Zloza A, Reiser
J, Shakhani SH.Overriding impaired FPR chemotaxis signaling
in diabetic neutrophil stimulates infection control in murine diabetic wound. Elife. 2022;11:e72071.
60. Colston J, Atkins B. Bone and joint infection. Clin Med.
2018;18(2):150.
61. Giurato L, Meloni M, Izzo V, Uccioli L. Osteomyelitis in
diabetic foot: a comprehensive overview. World J Diabetes.
2017;8(4):135–42.
62. Kremers HM, Nwojo ME, Ransom JE, Wood-Wentz CM, Melton
LJ III, Huddleston PM III.Trends in the epidemiology of osteomyelitis: a population-based study, 1969 to 2009. J Bone Joint
Surg Am. 2015;97(10):837.
63. Ahmad MA, Ab Rahman S, Islam MA.Prevalence and risk of
infection in patients with diabetes following primary total knee
arthroplasty: a global systematic review and meta-analysis of
120,754 knees. J Clin Med. 2022;11(13):3752.
64. Frydrych LM, Fattahi F, He K, Ward PA, Delano MJ. Diabetes
and sepsis: risk, recurrence, and ruination. Front Endocrinol.
2017;8:271.
65. Hillson R.The spine in diabetes. Pract Diab. 2018;35(1):5–6.
66. Lipsky BA, Berendt AR, Deery HG, Embil JM, Joseph WS,
Karchmer AW, LeFrock JL, Lew DP, Mader JT, Norden
C.Diagnosis and treatment of diabetic foot infections. Clin Infect
Dis. 2004;39:885–910.
67. Armstrong DG, Lipsky BA.Advances in the treatment of diabetic
foot infections. Diabetes Technol Ther. 2004;6(2):167–77.
68. Kaech C. The role of diabetes mellitus in patients with bloodstream infections. Swiss Med Wkly. 2008;138(3536):512.
69. McKane CK, Marmarelis M, Mendu ML, Moromizato T,
Gibbons FK, Christopher KB.Diabetes mellitus and communityacquired bloodstream infections in the critically ill. J Crit Care.
2014;29(1):70–6.
70. Rohani B.Oral manifestations in patients with diabetes mellitus.
World J Diabetes. 2019;10(9):485.
71. Taylor GW, Burt BA, Becker MP, Genco RJ, Shlossman M,
Knowler WC, Pettitt DJ.Severe periodontitis and risk for poor
glycemic control in patients with non-insulin-dependent diabetes
mellitus. J Periodontol. 1996;67:1085–93.
72. Indurkar MS, Maurya AS, Indurkar S.Oral manifestations of diabetes. Clin Diabetes. 2016;34(1):54–7.
73. Daniel R, Gokulanathan S, Shanmugasundaram N,
Lakshmigandhan M, Kavin T.Diabetes and periodontal disease.
J Pharm Bioallied Sci. 2012;4(Suppl 2):S280.
74. Martinez RFF, Jaimes-Aveldañez A, Hernández-Pérez F, Arenas
R, Miguel GF-S. Oral Candida spp. carriers: its prevalence
in patients with type 2 diabetes mellitus. An Bras Dermatol.
2013;88:222–5.
75. Chouhan S, Kallianpur S, Prabhu KT, Tijare M, Kasetty S, Gupta
S.Candidal prevalence in diabetics and its species identication.
Int J Appl Basic Med Res. 2019;9(1):49.
76. Khan T.Oral manifestations and complications of diabetes mellitus: a review. Int J Med Health Res. 2018;4:50–2.
77. Shakov R, Salazar RS, Kagunye SK, Baddoura WJ, DeBari
VA.Diabetes mellitus as a risk factor for recurrence of Clostridium
difcile infection in the acute care hospital setting. Am J Infect
Control. 2011;39(3):194–8.
78. Eliakim-Raz N, Fishman G, Yahav D, Goldberg E, Stein G, Zvi
H, Barsheshet A, Bishara J.Predicting Clostridium difcile infection in diabetic patients and the effect of metformin therapy: a
retrospective, case–control study. Eur J Clin Microbiol Infect Dis.
2015;34:1201–5.
79. Thomson S, Bade P, Taams M, Chrystal V.Gastrointestinal mucormycosis. Br J Surg. 1991;78(8):952–4.
80. Hammerstad SS, Grock SF, Lee HJ, Hasham A, Sundaram N,
Tomer Y.Diabetes and hepatitis C: a two-way association. Front
Endocrinol. 2015;6:134.
81. Chao A, Vazquez JA. Fungal infections of the gastrointestinal
tract. Gastroenterol Clin. 2021;50(2):243–60.
82. Safwan M, Penny SM. Emphysematous cholecystitis: a deadly
twist to a common disease. J Diagn Med Sonogr. 2016;32(3):131–7.
83. Antonelli A, Ferrari SM, Giuggioli D, Di Domenicantonio A,
Ruflli I, Corrado A, Fabiani S, Marchi S, Ferri C, Ferrannini
E.Hepatitis C virus infection and type 1 and type 2 diabetes mellitus. World J Diabetes. 2014;5(5):586.
84. Guo X, Jin M, Yang M, Liu K, Li J-w. Type 2 diabetes mellitus
and the risk of hepatitis C virus infection: a systematic review. Sci
Rep. 2013;3(1):2981.
85. Ndako JA, Owolabi AO, Olisa JA, Akinwumi JA, Dojumo VT,
Olatinsu O, Adebayo BA.Studies on the prevalence of hepatitis C
virus infection in diabetic patients attending a tertiary health-care
facility South-west Nigeria. BMC Infect Dis. 2020;20(1):1–10.
86. Inns T, Millership S, Teare L, Rice W, Reacher M.Service evaluation of selected risk factors for extended-spectrum beta-lactamase
Escherichia coli urinary tract infections: a case-control study. J
Hosp Infect. 2014;88(2):116–9.
87. Wu YH, Chen PL, Hung YP, Ko WC.Risk factors and clinical
impact of levooxacin or cefazolin nonsusceptibility or ESBL
production among uropathogens in adults with communityonset urinary tract infections. J Microbiol Immunol Infect.
2014;47(3):197–203.
88. Schechner V, Kotlovsky T, Kazma M, Mishali H, Schwartz D,
Navon-Venezia S, Schwaber MJ, Carmeli Y. Asymptomatic
rectal carriage of blaKPC producing carbapenem-resistant
Enterobacteriaceae: who is prone to become clinically infected?
Clin Microbiol Infect. 2013;19(5):451–6.
89. Papadimitriou-Olivgeris M, Drougka E, Fligou F, Kolonitsiou F,
Liakopoulos A, Dodou V, Anastassiou ED, Petinaki E, Marangos
M, Filos KS, Spiliopoulou I.Risk factors for enterococcal infection and colonization by vancomycin-resistant enterococci in critically ill patients. Infection. 2014;42(6):1013–22.
90. Sobel JD, Fisher JF, Kauffman CA, Newman CA.Candida urinary
tract infections—epidemiology. Clin Infect Dis. 2011;52(Suppl
6):S433–6.
91. Geerlings SE, Meiland R, van Lith EC, Brouwer EC, Gaastra W,
Hoepelman AI.Adherence of type 1-mbriated Escherichia coli
to uroepithelial cells: more in diabetic women than in control subjects. Diabetes Care. 2002;25(8):1405–9.
92. Goldufsky J, Wood S, Hajihossainlou B, Rehman T, Majdobeh
O, Kaufman HL, Ruby CE, Shakhani SH. Pseudomonas aeru-
ginosa exotoxin T induces potent cytotoxicity against a variety of
murine and human cancer cell lines. J Med Microbiol. 2015;64(Pt
2):164–73.
93. Colston J, Atkins B.Bone and joint infection. Clin Med (Lond).
2018;18(2):150–4.
94. Dryden M, Baguneid M, Eckmann C, Corman S, Stephens
J, Solem C, Li J, Charbonneau C, Baillon-Plot N, Haider
S.Pathophysiology and burden of infection in patients with diabetes mellitus and peripheral vascular disease: focus on skin and
soft-tissue infections. Clin Microbiol Infect. 2015;21:S27–32.
95. Macdonald KE, Boeckh S, Stacey HJ, Jones JD.The microbiology of diabetic foot infections: a meta-analysis. BMC Infect Dis.
2021;21(1):1–10.
96. Edmonds M, Manu C, Vas P.The current burden of diabetic foot
disease. J Clin Orthop Trauma. 2021;17:88–93.
97. Noor S, Zubair M, Ahmad J.Diabetic foot ulcer—a review on
pathophysiology, classication and microbial etiology. Diabetes
Metab Syndr Clin Res Rev. 2015;9(3):192–9.
98. Lipsky BA, Berendt AR, Cornia PB, Pile JC, Peters EJ, Armstrong
DG, Deery HG, Embil JM, Joseph WS, Karchmer AW. 2012
Infectious Diseases Society of America clinical practice guideline
320
https://t.me/med1917
R. Roy et al.
for the diagnosis and treatment of diabetic foot infections. Clin
Infect Dis. 2012;54(12):e132–73.
99. Atlaw A, Kebede HB, Abdela AA, Woldeamanuel Y.Bacterial isolates from diabetic foot ulcers and their antimicrobial resistance
prole from selected hospitals in Addis Ababa, Ethiopia. Front
Endocrinol. 2022;13:987487.
100. Saseedharan S, Sahu M, Chaddha R, Pathrose E, Bal A, Bhalekar
P, Sekar P, Krishnan P. Epidemiology of diabetic foot infections in a reference tertiary hospital in India. Braz J Microbiol.
2018;49:401–6.
101. Malik A, Mohammad Z, Ahmad J.The diabetic foot infections:
biolms and antimicrobial resistance. Diabetes Metab Syndr.
2013;7(2):101–7.
102. Ramakant P, Verma AK, Misra R, Prasad KN, Chand G, Mishra
A, Agarwal G, Agarwal A, Mishra SK.Changing microbiological prole of pathogenic bacteria in diabetic foot infections: time
for a rethink on which empirical therapy to choose? Diabetologia.
2011;54(1):58–64.
103. Dryden M, Baguneid M, Eckmann C, Corman S, Stephens
J, Solem C, Li J, Charbonneau C, Baillon-Plot N, Haider
S. Pathophysiology and burden of infection in patients with
diabetes mellitus and peripheral vascular disease: focus on skin
and soft-tissue infections. Clin Microbiol Infect. 2015;21(Suppl
2):S27–32.
104. Lipsky BA, Berendt AR, Cornia PB, Pile JC, Peters EJ, Armstrong
DG, Deery HG, Embil JM, Joseph WS, Karchmer AW, Pinzur MS,
Senneville E. 2012 Infectious Diseases Society of America clinical practice guideline for the diagnosis and treatment of diabetic
foot infections. Clin Infect Dis. 2012;54(12):e132–73.
105. Lipsky BA, Aragón-Sánchez J, Diggle M, Embil J, Kono S,
Lavery L, Senneville É, Urbančič-Rovan V, Van Asten S, Peters
EJ.IWGDF guidance on the diagnosis and management of foot
infections in persons with diabetes. Diabetes Metab Res Rev.
2016;32(Suppl 1):45–74.
106. Matthews PC, Berendt AR, Lipsky BA.Clinical management of
diabetic foot infection: diagnostics, therapeutics and the future.
Expert Rev Anti-Infect Ther. 2007;5(1):117–27.
107. Lamloum SM, Mobasher LA, Karar AH, Basiony L, Abdallah
TH, Al-Saleh AI, Al-Shamali NA.Relationship between postoperative infectious complications and glycemic control for diabetic
patients in an orthopedic hospital in Kuwait. Med Princ Pract.
2009;18(6):447–52.
108. Redel H, Gao Z, Li H, Alekseyenko AV, Zhou Y, Perez-Perez GI,
Weinstock G, Sodergren E, Blaser MJ.Quantitation and composition of cutaneous microbiota in diabetic and nondiabetic men. J
Infect Dis. 2013;207(7):1105–14.
109. Jneid J, Lavigne J, La Scola B, Cassir N.The diabetic foot microbiota: a review. Hum Microbiome J. 2017;5:1–6.
110. Steglińska A, Jachowicz A, Szulc J, Adamiak J, Otlewska A,
Pielech-Przybylska K, Gutarowska B.Factors inuencing microbiological biodiversity of human foot skin. Int J Environ Res
Public Health. 2019;16(18):3503.
111. Adamczyk K, Garncarczyk A, Antończak P, Wcisło-Dziadecka
D.The foot microbiome. J Cosmet Dermatol. 2020;19(5):1039–43.
112. Grice EA, Segre JA.The skin microbiome. Nat Rev Microbiol.
2011;9(4):244–53.
113. Gardiner M, Vicaretti M, Sparks J, Bansal S, Bush S, Liu M,
Darling A, Harry E, Burke CM.A longitudinal study of the diabetic skin and wound microbiome. PeerJ. 2017;5:e3543.
114. Grice EA, Snitkin ES, Yockey LJ, Bermudez DM, Liechty KW,
Segre JA.Longitudinal shift in diabetic wound microbiota correlates with prolonged skin defense response. Proc Natl Acad Sci
U S A. 2010;107(33):14799–804.
115. Kalan LR, Meisel JS, Loesche MA, Horwinski J, Soaita I, Chen
X, Uberoi A, Gardner SE, Grice EA.Strain- and species-level
variation in the microbiome of diabetic wounds is associated with
clinical outcomes and therapeutic efcacy. Cell Host Microbe.
2019;25(5):641–655.e5.
116. Bjarnsholt T, Kirketerp-Moller K, Jensen PO, Madsen KG, Phipps
R, Krogfelt K, Hoiby N, Givskov M.Why chronic wounds will not
heal: a novel hypothesis. Wound Repair Regen. 2008;16(1):2–10.
117. Gjodsbol K, Christensen JJ, Karlsmark T, Jorgensen B, Klein BM,
Krogfelt KA.Multiple bacterial species reside in chronic wounds:
a longitudinal study. Int Wound J. 2006;3(3):225–31.
118. Madsen SM, Westh H, Danielsen L, Rosdahl VT. Bacterial
colonization and healing of venous leg ulcers. APMIS.
1996;104(12):895–9.
119. Oyibo SO, Jude EB, Tarawneh I, Nguyen HC, Armstrong DG,
Harkless LB, Boulton AJ. The effects of ulcer size and site,
patient’s age, sex and type and duration of diabetes on the outcome of diabetic foot ulcers. Diabet Med. 2001;18(2):133–8.
120. Mendes JJ, Leandro CI, Bonaparte DP, Pinto AL.A rat model of
diabetic wound infection for the evaluation of topical antimicrobial therapies. Comp Med. 2012;62(1):37–48.
121. Schierle CF, De la Garza M, Mustoe TA, Galiano
RD.Staphylococcal biolms impair wound healing by delaying
reepithelialization in a murine cutaneous wound model. Wound
Repair Regen. 2009;17(3):354–9.
122. Pastar I, Sawaya AP, Marjanovic J, Burgess JL, Strbo N, Rivas KE,
Wikramanayake TC, Head CR, Stone RC, Jozic I.Intracellular
Staphylococcus aureus triggers pyroptosis and contributes to
inhibition of healing due to perforin-2 suppression. J Clin Invest.
2021;131(24):e133727.
123. Sotto A, Lina G, Richard J-L, Combescure C, Bourg G, Vidal
L, Jourdan N, Etienne J, Lavigne J-P. Virulence potential of
Staphylococcus aureus strains isolated from diabetic foot ulcers: a
new paradigm. Diabetes Care. 2008;31(12):2318–24.
124. Gubara Musa H, Ahmed ME.Associated risk factors and management of chronic diabetic foot ulcers exceeding 6 months’ duration.
Diabet Foot Ankle. 2012;3(1):18980.
125. Park S, Rich J, Hanses F, Lee JC. Defects in innate immunity predispose C57BL/6J-Leprdb/Leprdb mice to infection by
Staphylococcus aureus. Infect Immun. 2009;77(3):1008–14.
126. Afonso AC, Oliveira D, Saavedra MJ, Borges A, Simões
M.Biolms in diabetic foot ulcers: impact, risk factors and control strategies. Int J Mol Sci. 2021;22(15):8278.
127. Flemming H-C, Wingender J. The biolm matrix. Nat Rev
Microbiol. 2010;8(9):623–33.
128. Vestby LK, Grønseth T, Simm R, Nesse LL.Bacterial biolm and
its role in the pathogenesis of disease. Antibiotics. 2020;9(2):59.
129. Adler AI, Boyko EJ, Ahroni JH, Smith DG. Lower-extremity
amputation in diabetes. The independent effects of peripheral vascular disease, sensory neuropathy, and foot ulcers. Diabetes Care.
1999;22(7):1029–35.
130. Versey Z, da Cruz Nizer WS, Russell E, Zigic S, DeZeeuw KG,
Marek JE, Overhage J, Cassol E.Biolm-innate immune interface: contribution to chronic wound formation. Front Immunol.
2021;12:648554.
131. Tankersley A, Frank MB, Bebak M, Brennan R. Early effects
of Staphylococcus aureus biolm secreted products on inammatory responses of human epithelial keratinocytes. J Inamm.
2014;11:1–11.
132. González JF, Hahn MM, Gunn JS. Chronic biolm-based
infections: skewing of the immune response. Pathog Dis.
2018;76(3):fty023.
133. Zhao G, Usui ML, Underwood RA, Singh PK, James GA, Stewart
PS, Fleckman P, Olerud JE.Time course study of delayed wound
healing in a biolm-challenged diabetic mouse model. Wound
Repair Regen. 2012;20(3):342–52.
134. Nguyen AT, Oglesby-Sherrouse AG. Interactions between
Pseudomonas aeruginosa and Staphylococcus aureus during
17 Infection inDiabetes: Epidemiology, Immune Dysfunctions, andTherapeutics
https://t.me/med1917
321
co-cultivations and polymicrobial infections. Appl Microbiol
Biotechnol. 2016;100:6141–8.
135. Zhao G, Hochwalt PC, Usui ML, Underwood RA, Singh PK,
James GA, Stewart PS, Fleckman P, Olerud JE.Delayed wound
healing in diabetic (db/db) mice with Pseudomonas aeruginosa
biolm challenge: a model for the study of chronic wounds.
Wound Repair Regen. 2010;18(5):467–77.
136. Shakhani SH, Morales C, Engel J.The Pseudomonas aeruginosa
type III secreted toxin ExoT is necessary and sufcient to induce
apoptosis in epithelial cells. Cell Microbiol. 2008;10(4):994–1007.
137. Wood SJ, Goldufsky J, Shakhani SH. Pseudomonas aeruginosa
ExoT induces atypical anoikis apoptosis in target host cells by
transforming Crk adaptor protein into a cytotoxin. PLoS Pathog.
2015;11(5):e1004934.
138. Wood SJ, Goldufsky JW, Bello D, Masood S, Shakhani
SH. Pseudomonas aeruginosa ExoT induces mitochondrial
apoptosis in target host cells in a manner that depends on its
GTPase-activating protein (GAP) domain activity. J Biol Chem.
2015;290(48):29063–73.
139. Kaminski A, Gupta KH, Goldufsky JW, Lee HW, Gupta V,
Shakhani SH. Pseudomonas aeruginosa ExoS induces intrinsic
apoptosis in target host cells in a manner that is dependent on its
GAP domain activity. Sci Rep. 2018;8(1):14047.
140. Wood SJ, Goldufsky JW, Seu MY, Dorafshar AH, Shakhani SH.
Pseudomonas aeruginosa cytotoxins: mechanisms of cytotoxicity and impact on inammatory responses. Cells. 2023;12(1):195.
141. Otto M. Staphylococcus aureus toxins. Curr Opin Microbiol.
2014;17:32–7.
142. DuMont AL, Nygaard TK, Watkins RL, Smith A, Kozhaya
L, Kreiswirth BN, Shopsin B, Unutmaz D, Voyich JM,
Torres VJ. Characterization of a new cytotoxin that contributes to Staphylococcus aureus pathogenesis. Mol Microbiol.
2011;79(3):814–25.
143. Wood S, Pithadia R, Rehman T, Zhang L, Plichta J, Radek KA,
Forsyth C, Keshavarzian A, Shakhani SH. Chronic alcohol
exposure renders epithelial cells vulnerable to bacterial infection.
PLoS One. 2013;8(1):e54646.
144. Tkaczyk C, Jones-Nelson O, Shi YY, Tabor DE, Cheng L, Zhang
T, Sellman BR. Neutralizing Staphylococcus aureus virulence
with AZD6389, a three mAb combination, accelerates closure of
a diabetic polymicrobial wound. Msphere. 2022;7(3):e00130–22.
145. Mohamed MF, Gupta K, Goldufsky JW, Roy R, Callaghan LT,
Wetzel DM, Kuzel TM, Reiser J, Shakhani SH.CrkII/Abl phosphorylation cascade is critical for NLRC4 inammasome activity
and is blocked by Pseudomonas aeruginosa ExoT.Nat Commun.
2022;13(1):1–16.
146. Athanasopoulos AN, Economopoulou M, Orlova VV, Sobke A,
Schneider D, Weber H, Augustin HG, Eming SA, Schubert U, Linn
T, Nawroth PP, Hussain M, Hammes HP, Herrmann M, Preissner
KT, Chavakis T. The extracellular adherence protein (Eap) of
Staphylococcus aureus inhibits wound healing by interfering with
host defense and repair mechanisms. Blood. 2006;107(7):2720–7.
147. Chen H, Zhang J, He Y, Lv Z, Liang Z, Chen J, Li P, Liu J, Yang
H, Tao A.Exploring the role of Staphylococcus aureus in inammatory diseases. Toxins. 2022;14(7):464.
148. Mohamed MF, Wood SJ, Roy R, Reiser J, Kuzel TM, Shakhani
SH. Pseudomonas aeruginosa ExoT induces G1 cell cycle arrest
in melanoma cells. Cell Microbiol. 2021;23(8):e13339.
149. Shakhani SH, Engel J. Pseudomonas aeruginosa type III-secreted
toxin ExoT inhibits host-cell division by targeting cytokinesis at
multiple steps. Proc Natl Acad Sci U S A. 2006;103(42):15605–10.
150. Tran PM, Tang SS, Salgado-Pabón W. Staphylococcus
aureus β-toxin exerts anti-angiogenic effects by inhibiting reendothelialization and neovessel formation. Front Microbiol.
2022;13:840236.
151. Prasad ASB, Shruptha P, Prabhu V, Srujan C, Nayak UY,
Anuradha CKR, Ramachandra L, Keerthana P, Joshi MB, Murali
TS. Pseudomonas aeruginosa virulence proteins pseudolysin
and protease IV impede cutaneous wound healing. Lab Investig.
2020;100(12):1532–50.
152. Martin A, Komada MR, Sane DC.Abnormal angiogenesis in diabetes mellitus. Med Res Rev. 2003;23(2):117–45.
153. Rai V, Moellmer R, Agrawal DK.Stem cells and angiogenesis:
implications and limitations in enhancing chronic diabetic foot
ulcer healing. Cells. 2022;11(15):2287.
154. Wood SJ, Kuzel TM, Shakhani SH. Pseudomonas aerugi-
nosa: infections, animal modeling, and therapeutics. Cells.
2023;12(1):199.
155. Cohen TS, Takahashi V, Bonnell J, Tovchigrechko A, Chaerkady
R, Yu W, Jones-Nelson O, Lee Y, Raja R, Hess S.Staphylococcus
aureus drives expansion of low-density neutrophils in diabetic
mice. J Clin Invest. 2019;129(5):2133–44.
156. Mahmood F, Hakimiyan A, Jayaraman V, Wood S,
Sivaramakrishnan G, Rehman T, Reuhs BL, Chubinskaya S,
Shakhani SH. A novel human antimicrobial factor targets
Pseudomonas aeruginosa through its type III secretion system. J
Med Microbiol. 2013;62(Pt 4):531–9.
157. MacLeod AS, Mansbridge JN.The innate immune system in acute
and chronic wounds. Adv Wound Care. 2016;5(2):65–78.
158. McDonald DR, Levy O.Innate immunity. In: Clinical immunology. Elsevier; 2019. p.39–53.e1.
159. Martin P, Leibovich SJ. Inammatory cells during wound
repair: the good, the bad and the ugly. Trends Cell Biol.
2005;15(11):599–607.
160. Wilkinson HN, Hardman MJ. Wound healing: cellular mechanisms and pathological outcomes. Open Biol. 2020;10(9):200223.
161. Wallace HA, Basehore BM, Zito PM. Wound healing phases.
Treasure Island, FL: StatPearls Publishing; 2017.
162. Kim M-H, Liu W, Borjesson DL, Curry F-RE, Miller LS, Cheung
AL, Liu F-T, Isseroff RR, Simon SI.Dynamics of neutrophil inltration during cutaneous wound healing and infection using uorescence imaging. J Invest Dermatol. 2008;128(7):1812–20.
163. Velnar T, Bailey T, Smrkolj V. The wound healing process: an
overview of the cellular and molecular mechanisms. J Int Med
Res. 2009;37(5):1528–42.
164. Fenteany G, Janmey PA, Stossel TP.Signaling pathways and cell
mechanics involved in wound closure by epithelial cell sheets.
Curr Biol. 2000;10(14):831–8.
165. Schafer M, Werner S. Cancer as an overhealing wound: an old
hypothesis revisited. Nat Rev Mol Cell Biol. 2008;9(8):628–38.
166. Martin P.Wound healing—aiming for perfect skin regeneration.
Science. 1997;276(5309):75–81.
167. Diegelmann RF, Evans MC.Wound healing: an overview of acute,
brotic and delayed healing. Front Biosci. 2004;9:283–9.
168. Roy R, Zayas J, Mohamed MF, Aboonabi A, Delgado K, Wallace
J, Bayat M, Kuzel TM, Reiser J, Shakhani SH.IL-10 dysregulation underlies chemokine insufciency, delayed macrophage
response, and impaired healing in diabetic wounds. J Invest
Dermatol. 2022;142(3):692–704.e14.
169. Wood S, Jayaraman V, Huelsmann EJ, Bonish B, Burgad D,
Sivaramakrishnan G, Qin S, Dipietro LA, Zloza A, Zhang C,
Shakhani SH. Pro-inammatory chemokine CCL2 (MCP-1)
promotes healing in diabetic wounds by restoring the macrophage
response. PLoS One. 2014;9(3):e91574.
170. de Oliveira S, Rosowski EE, Huttenlocher A.Neutrophil migration in infection and wound repair: going forward in reverse. Nat
Rev Immunol. 2016;16(6):378–91.
171. Liu M, Chen K, Yoshimura T, Liu Y, Gong W, Wang A, Gao J-L,
Murphy PM, Wang JM.Formylpeptide receptors are critical for
rapid neutrophil mobilization in host defense against Listeria
monocytogenes. Sci Rep. 2012;2:786.
172. Sadik CD, Kim ND, Luster AD.Neutrophils cascading their way
to inammation. Trends Immunol. 2011;32(10):452–60.
322
https://t.me/med1917
R. Roy et al.
173. Futosi K, Fodor S, Mocsai A. Neutrophil cell surface receptors and their intracellular signal transduction pathways. Int
Immunopharmacol. 2013;17(3):638–50.
174. Ng LG, Qin JS, Roediger B, Wang Y, Jain R, Cavanagh LL, Smith
AL, Jones CA, De Veer M, Grimbaldeston MA. Visualizing
the neutrophil response to sterile tissue injury in mouse dermis reveals a three-phase cascade of events. J Invest Dermatol.
2011;131(10):2058–68.
175. Afonso PV, Janka-Junttila M, Lee YJ, McCann CP, Oliver CM,
Aamer KA, Losert W, Cicerone MT, Parent CA. LTB4 is a
signal- relay molecule during neutrophil chemotaxis. Dev Cell.
2012;22(5):1079–91.
176. Chou RC, Kim ND, Sadik CD, Seung E, Lan Y, Byrne MH,
Haribabu B, Iwakura Y, Luster AD. Lipid-cytokine-chemokine
cascade drives neutrophil recruitment in a murine model of
inammatory arthritis. Immunity. 2010;33(2):266–78.
177. Roupe KM, Nybo M, Sjobring U, Alberius P, Schmidtchen
A, Sorensen OE.Injury is a major inducer of epidermal innate
immune responses during wound healing. J Invest Dermatol.
2010;130(4):1167–77.
178. Mowat AG, Baum J. Chemotaxis of polymorphonuclear leukocytes from patients with diabetes mellitus. N Engl J Med.
1971;284(12):621–7.
179. Delamaire M, Maugendre D, Moreno M, Le Goff MC, Allannic
H, Genetet B.Impaired leucocyte functions in diabetic patients.
Diabet Med. 1997;14(1):29–34.
180. Nie L, Zhao P, Yue Z, Zhang P, Ji N, Chen Q, Wang Q.Diabetes
induces macrophage dysfunction through cytoplasmic dsDNA/
AIM2 associated pyroptosis. J Leukoc Biol. 2021;110(3):497–510.
181. Geerlings SE, Hoepelman AI. Immune dysfunction in patients
with diabetes mellitus (DM). FEMS Immunol Med Microbiol.
1999;26(3–4):259–65.
182. Galkowska H, Wojewodzka U, Olszewski WL.Low recruitment
of immune cells with increased expression of endothelial adhesion
molecules in margins of the chronic diabetic foot ulcers. Wound
Repair Regen. 2005;13(3):248–54.
183. Sawaya AP, Stone RC, Brooks SR, Pastar I, Jozic I, Hasneen
K, O’Neill K, Mehdizadeh S, Head CR, Strbo N. Deregulated
immune cell recruitment orchestrated by FOXM1 impairs human
diabetic wound healing. Nat Commun. 2020;11(1):1–14.
184. Wetzler C, Kampfer H, Stallmeyer B, Pfeilschifter J, Frank
S.Large and sustained induction of chemokines during impaired
wound healing in the genetically diabetic mouse: prolonged persistence of neutrophils and macrophages during the late phase of
repair. J Invest Dermatol. 2000;115(2):245–53.
185. Galkina E, Ley K.Vascular adhesion molecules in atherosclerosis.
Arterioscler Thromb Vasc Biol. 2007;27(11):2292–301.
186. Herter JM, Rossaint J, Spieker T, Zarbock A.Adhesion molecules
involved in neutrophil recruitment during sepsis-induced acute
kidney injury. J Innate Immun. 2014;6(5):597–606.
187. Rainger GE, Buckley C, Simmons DL, Nash GB. Cross-talk
between cell adhesion molecules regulates the migration velocity
of neutrophils. Curr Biol. 1997;7(5):316–25.
188. Meigs JB, Hu FB, Rifai N, Manson JE. Biomarkers of endothelial dysfunction and risk of type 2 diabetes mellitus. JAMA.
2004;291(16):1978–86.
189. Chen L, DiPietro LA.Toll-like receptor function in acute wounds.
Adv Wound Care. 2017;6(10):344–55.
190. Weinheimer-Haus EM, Mirza RE, Koh TJ.Nod-like receptor protein- 3 inammasome plays an important role during early stages
of wound healing. PLoS One. 2015;10(3):e0119106.
191. Artlett CM. Inammasomes in wound healing and brosis. J
Pathol. 2013;229(2):157–67.
192. Dasu MR, Martin SJ.Toll-like receptor expression and signaling
in human diabetic wounds. World J Diabetes. 2014;5(2):219.
193. Dasu MR, Devaraj S, Park S, Jialal I.Increased toll-like receptor
(TLR) activation and TLR ligands in recently diagnosed type 2
diabetic subjects. Diabetes Care. 2010;33(4):861–8.
194. Cavalcante-Silva J, Koh TJ. Targeting the NOD-like receptor
Pyrin domain containing 3 inammasome to improve healing of
diabetic wounds. Adv Wound Care. 2023;12(11):644–56.
195. Sun X, Wang X, Zhao Z, Chen J, Li C, Zhao G. Paeoniorin
inhibited nod-like receptor protein-3 inammasome and
NF-κB-mediated inammatory reactions in diabetic foot ulcer
by inhibiting the chemokine receptor CXCR2. Drug Dev Res.
2021;82(3):404–11.
196. Ishida Y, Kuninaka Y, Nosaka M, Furuta M, Kimura A, Taruya
A, Yamamoto H, Shimada E, Akiyama M, Mukaida N. CCL2mediated reversal of impaired skin wound healing in diabetic mice
by normalization of neovascularization and collagen accumulation. J Invest Dermatol. 2019;139(12):2517–2527.e5.
197. Kaymakcalan OE, Abadeer A, Goldufsky JW, Galili U, Karinja
SJ, Dong X, Jin JL, Samadi A, Spector JA. Topical α-gal
nanoparticles accelerate diabetic wound healing. Exp Dermatol.
2020;29(4):404–13.
198. Srinivasan D, Plattner R.Activation of Abl tyrosine kinases promotes invasion of aggressive breast cancer cells. Cancer Res.
2006;66(11):5648–55.
199. Honnegowda TM, Kumar P, Udupa EGP, Kumar S, Kumar U,
Rao P.Role of angiogenesis and angiogenic factors in acute and
chronic wound healing. Plast Aesthet Res. 2015;2:243–9.
200. Schulz C, Perdiguero EG, Chorro L, Szabo-Rogers H, Cagnard
N, Kierdorf K, Prinz M, Wu B, Jacobsen SEW, Pollard JW.A lineage of myeloid cells independent of Myb and hematopoietic stem
cells. Science. 2012;336(6077):86–90.
201. Okonkwo UA, DiPietro LA.Diabetes and wound angiogenesis.
Int J Mol Sci. 2017;18(7):1419.
202. Dinh T, Veves A.Microcirculation of the diabetic foot. Curr Pharm
Des. 2005;11(18):2301–9.
203. Wang J.Neutrophils in tissue injury and repair. Cell Tissue Res.
2018;371:531–9.
204. Kim SY, Nair MG.Macrophages in wound healing: activation and
plasticity. Immunol Cell Biol. 2019;97(3):258–67.
205. Kloc M, Ghobrial RM, Wosik J, Lewicka A, Lewicki S, Kubiak
JZ.Macrophage functions in wound healing. J Tissue Eng Regen
Med. 2019;13(1):99–109.
206. Teng T-S, Ji A-L, Ji X-Y, Li Y-Z. Neutrophils and immunity:
from bactericidal action to being conquered. J Immunol Res.
2017;2017:1.
207. Dovi JV, Szpaderska AM, DiPietro LA.Neutrophil function in
the healing wound: adding insult to injury? Thromb Haemost.
2004;92(2):275–80.
208. Brinkmann V, Reichard U, Goosmann C, Fauler B, Uhlemann Y,
Weiss DS, Weinrauch Y, Zychlinsky A.Neutrophil extracellular
traps kill bacteria. Science. 2004;303(5663):1532–5.
209. Aderem A, Underhill DM.Mechanisms of phagocytosis in macrophages. Annu Rev Immunol. 1999;17:593–623.
210. Sasada M, Johnston RB. Macrophage microbicidal activity.
Correlation between phagocytosis-associated oxidative metabolism and the killing of Candida by macrophages. J Exp Med.
1980;152(1):85–98.
211. Helmy KY, Katschke KJ, Gorgani NN, Kljavin NM, Elliott JM,
Diehl L, Scales SJ, Ghilardi N, van Lookeren Campagne M.CRIg:
a macrophage complement receptor required for phagocytosis of
circulating pathogens. Cell. 2006;124(5):915–27.
212. Doster RS, Rogers LM, Gaddy JA, Aronoff DM. Macrophage
extracellular traps: a scoping review. J Innate Immun.
2018;10(1):3–13.
213. Doster RS, Sutton JA, Rogers LM, Aronoff DM, Gaddy
JA. Streptococcus agalactiae induces placental macrophages
to release extracellular traps loaded with tissue remodeling
enzymes via an oxidative burst-dependent mechanism. MBio.
2018;9(6):e02084–18.
214. Weng W, Hu Z, Pan Y. Macrophage extracellular traps: current
opinions and the state of research regarding various diseases. J
Immunol Res. 2022;2022:7050807.
17 Infection inDiabetes: Epidemiology, Immune Dysfunctions, andTherapeutics
https://t.me/med1917
323
215. Wilson R, Tomlinson D, Reeves W. Neutrophil sorbitol production impairs oxidative killing in diabetes. Diabet Med.
1987;4(1):37–40.
216. Pavlou S, Lindsay J, Ingram R, Xu H, Chen M.Sustained high
glucose exposure sensitizes macrophage responses to cytokine
stimuli but reduces their phagocytic activity. BMC Immunol.
2018;19(1):1–13.
217. Repine JE, Clawson C, Goetz FC.Bactericidal function of neutrophils from patients with acute bacterial infections and from diabetics. J Infect Dis. 1980;142(6):869–75.
218. Lee WL, Harrison RE, Grinstein S.Phagocytosis by neutrophils.
Microbes Infect. 2003;5(14):1299–306.
219. Uribe-Querol E, Rosales C. Phagocytosis: our current understanding of a universal biological process. Front Immunol.
2020;11:1066.
220. Huang J, Xiao Y, Xu A, Zhou Z.Neutrophils in type 1 diabetes. J
Diabetes Investig. 2016;7(5):652–63.
221. Mancuso P, Gottschalk A, Phare SM, Peters-Golden M, Lukacs
NW, Huffnagle GB. Leptin-decient mice exhibit impaired
host defense in Gram-negative pneumonia. J Immunol.
2002;168(8):4018–24.
222. Uccioli L, Sinistro A, Almerighi C, Ciaprini C, Cavazza A, Giurato
L, Ruotolo V, Spasaro F, Vainieri E, Rocchi G.Proinammatory
modulation of the surface and cytokine phenotype of monocytes in patients with acute Charcot foot. Diabetes Care.
2010;33(2):350–5.
223. Jafar N, Edriss H, Nugent K. The effect of short-term hyperglycemia on the innate immune system. Am J Med Sci.
2016;351(2):201–11.
224. Martinez N, Ketheesan N, West K, Vallerskog T, Kornfeld
H. Impaired recognition of Mycobacterium tuberculosis
by alveolar macrophages from diabetic mice. J Infect Dis.
2016;214(11):1629–37.
225. Cancello R, Henegar C, Viguerie N, Taleb S, Poitou C, Rouault C,
Coupaye M, Pelloux V, Hugol D, Bouillot J-L.Reduction of macrophage inltration and chemoattractant gene expression changes
in white adipose tissue of morbidly obese subjects after surgeryinduced weight loss. Diabetes. 2005;54(8):2277–86.
226. Roos D, van Bruggen R, Meischl C.Oxidative killing of microbes
by neutrophils. Microbes Infect. 2003;5(14):1307–15.
227. Vazquez-Torres A, Jones-Carson J, Mastroeni P, Ischiropoulos H,
Fang FC.Antimicrobial actions of the NADPH phagocyte oxidase
and inducible nitric oxide synthase in experimental salmonellosis. I.Effects on microbial killing by activated peritoneal macrophages invitro. J Exp Med. 2000;192(2):227–36.
228. Alba-Loureiro TC, Munhoz C, Martins J, Cerchiaro G, Scavone
C, Curi R, Sannomiya P. Neutrophil function and metabolism
in individuals with diabetes mellitus. Braz J Med Biol Res.
2007;40:1037–44.
229. Marhoffer W, Stein M, Schleinkofer L, Federlin K. Evidence
of exvivo and invitro impaired neutrophil oxidative burst and
phagocytic capacity in type 1 diabetes mellitus. Diabetes Res Clin
Pract. 1993;19(3):183–8.
230. Mohsenin V, Latifpour J. Respiratory burst in alveolar macrophages of diabetic rats. J Appl Physiol. 1990;68(6):2384–90.
231. Mortaz E, Alipoor SD, Adcock IM, Mumby S, Koenderman
L.Update on neutrophil function in severe inammation. Front
Immunol. 2018;9:2171.
232. Sheshachalam A, Srivastava N, Mitchell T, Lacy P, Eitzen
G.Granule protein processing and regulated secretion in neutrophils. Front Immunol. 2014;5:448.
233. Borregaard N, Cowland JB.Granules of the human neutrophilic
polymorphonuclear leukocyte. Blood. 1997;89(10):3503–21.
234. Nolan CM, Beaty HN, Bagdade JD.Further characterization of
the impaired bactericidal function of granulocytes in patients with
poorly controlled diabetes. Diabetes. 1978;27(9):889–94.
235. Stegenga ME, van der Crabben SN, Blümer RM, Levi M,
Meijers JC, Serlie MJ, Tanck MW, Sauerwein HP, van der Poll
T.Hyperglycemia enhances coagulation and reduces neutrophil
degranulation, whereas hyperinsulinemia inhibits brinolysis during human endotoxemia. Blood. 2008;112(1):82–9.
236. Zhu S, Yu Y, Ren Y, Xu L, Wang H, Ling X, Jin L, Hu Y, Zhang
H, Miao C.The emerging roles of neutrophil extracellular traps in
wound healing. Cell Death Dis. 2021;12(11):984.
237. Andrews RK, Arthur JF, Gardiner EE. Neutrophil extracellular traps (NETs) and the role of platelets in infection. Thromb
Haemost. 2014;112(10):659–65.
238. Yipp BG, Petri B, Salina D, Jenne CN, Scott BN, Zbytnuik LD,
Pittman K, Asaduzzaman M, Wu K, Meijndert HC. Infectioninduced NETosis is a dynamic process involving neutrophil multitasking invivo. Nat Med. 2012;18(9):1386–93.
239. Li T, Zhang Z, Li X, Dong G, Zhang M, Xu Z, Yang J.Neutrophil
extracellular traps: signaling properties and disease relevance.
Mediat Inamm. 2020;2020:1.
240. Carestia A, Frechtel G, Cerrone G, Linari MA, Gonzalez CD,
Casais P, Schattner M. NETosis before and after hyperglycemic control in type 2 diabetes mellitus patients. PLoS One.
2016;11(12):e0168647.
241. Wong SL, Demers M, Martinod K, Gallant M, Wang Y, Goldne
AB, Kahn CR, Wagner DD. Diabetes primes neutrophils to
undergo NETosis, which impairs wound healing. Nat Med.
2015;21(7):815–9.
242. Fadini GP, Menegazzo L, Rigato M, Scattolini V, Poncina N,
Bruttocao A, Ciciliot S, Mammano F, Ciubotaru CD, Brocco
E.NETosis delays diabetic wound healing in mice and humans.
Diabetes. 2016;65(4):1061–71.
243. Njeim R, Azar WS, Fares AH, Azar ST, Kassouf HK, Eid
AA.NETosis contributes to the pathogenesis of diabetes and its
complications. J Mol Endocrinol. 2020;65(4):R65–76.
244. Prager I, Watzl C.Mechanisms of natural killer cell-mediated cellular cytotoxicity. J Leukoc Biol. 2019;105(6):1319–29.
245. Trapani JA, Smyth MJ.Functional signicance of the perforin/granzyme cell death pathway. Nat Rev Immunol. 2002;2(10):735–47.
246. Vivier E, Raulet DH, Moretta A, Caligiuri MA, Zitvogel L, Lanier
LL, Yokoyama WM, Ugolini S.Innate or adaptive immunity? The
example of natural killer cells. Science. 2011;331(6013):44–9.
247. Nimmerjahn F, Ravetch JV.Fcγ receptors as regulators of immune
responses. Nat Rev Immunol. 2008;8(1):34–47.
248. Hodgson K, Morris J, Bridson T, Govan B, Rush C, Ketheesan
N.Immunological mechanisms contributing to the double burden
of diabetes and intracellular bacterial infections. Immunology.
2015;144(2):171–85.
249. Berrou J, Fougeray S, Venot M, Chardiny V, Gautier J-F, Dulphy
N, Toubert A, Peraldi M-N.Natural killer cell function, an important target for infection and tumor protection, is impaired in type 2
diabetes. PLoS One. 2013;8(4):e62418.
250. O’Shea D, Hogan AE.Dysregulation of natural killer cells in obesity. Cancers. 2019;11(4):573.
251. Zhang Q-Y, Yan Z-B, Meng Y-M, Hong X-Y, Shao G, Ma J-J,
Cheng X-R, Liu J, Kang J, Fu C-Y. Antimicrobial peptides:
mechanism of action, activity and clinical potential. Mil Med Res.
2021;8:1–25.
252. Mangoni ML, McDermott AM, Zasloff M.Antimicrobial peptides
and wound healing: biological and therapeutic considerations.
Exp Dermatol. 2016;25(3):167–73.
253. Luo Y, Song Y.Mechanism of antimicrobial peptides: antimicrobial, anti-inammatory and antibiolm activities. Int J Mol Sci.
2021;22(21):11401.
254. Kang S-J, Park SJ, Mishig-Ochir T, Lee B-J. Antimicrobial
peptides: therapeutic potentials. Expert Rev Anti Infect Ther.
2014;12(12):1477–86.
324
https://t.me/med1917
R. Roy et al.
255. Selsted ME, Ouellette AJ.Mammalian defensins in the antimicrobial immune response. Nat Immunol. 2005;6(6):551–7.
256. Zanetti M.The role of cathelicidins in the innate host defenses of
mammals. Curr Issues Mol Biol. 2005;7(2):179–96.
257. Kavanagh K, Dowd S.Histatins: antimicrobial peptides with therapeutic potential. J Pharm Pharmacol. 2004;56(3):285–9.
258. Shah D, Son K-N, Kalmodia S, Lee B-S, Ali M, Balasubramaniam
A, Shukla D, Aakalu VK. Wound healing properties of
histatin-5 and identication of a functional domain required for
histatin-5-induced cell migration. Mol Ther Methods Clin Dev.
2020;17:709–16.
259. Rivas-Santiago B, Trujillo V, Montoya A, Gonzalez-Curiel I,
Castaneda-Delgado J, Cardenas A, Rincon K, Hernandez ML,
Hernandez-Pando R.Expression of antimicrobial peptides in diabetic foot ulcer. J Dermatol Sci. 2012;65(1):19–26.
260. Gonzalez-Curiel I, Trujillo V, Montoya-Rosales A, Rincon
K, Rivas-Calderon B, deHaro-Acosta J, Marin-Luevano P,
Lozano- Lopez D, Enciso-Moreno JA, Rivas-Santiago B.
1,25- dihydroxyvitamin D3 induces LL-37 and HBD-2 production
in keratinocytes from diabetic foot ulcers promoting wound healing: an invitro model. PLoS One. 2014;9(10):e111355.
261. Linn O, Menges B, Lammert F, Weber SN, Krawczyk M.Altered
expression of antimicrobial peptides in the upper gastrointestinal
tract of patients with diabetes mellitus. Nutrients. 2023;15(3):754.
262. Mohanty S, Kamolvit W, Scheffschick A, Björklund A, Tovi
J, Espinosa A, Brismar K, Nyström T, Schröder JM, Östenson
C-G.Diabetes downregulates the antimicrobial peptide psoriasin
and increases E. coli burden in the urinary bladder. Nat Commun.
2022;13(1):4983.
263. Galkowska H, Olszewski WL, Wojewodzka U. Expression of
natural antimicrobial peptide beta-defensin-2 and Langerhans cell
accumulation in epidermis from human non-healing leg ulcers.
Folia Histochem Cytobiol. 2005;43(3):133–6.
264. Sanchez A, Reeser J, Lau H, Yahiku P, Willard R, McMillan P,
Cho S, Magie A, Register UD.Role of sugars in human neutrophilic phagocytosis. Am J Clin Nutr. 1973;26(11):1180–4.
265. Lecube A, Pachón G, Petriz J, Hernández C, Simó R.Phagocytic
activity is impaired in type 2 diabetes mellitus and increases after
metabolic improvement. PLoS One. 2011;6(8):e23366.
266. Lan CC, Wu CS, Huang SM, Kuo HY, Wu IH, Liang CW, Chen
GS. High-glucose environment reduces human beta-defensin-2
expression in human keratinocytes: implications for poor diabetic
wound healing. Br J Dermatol. 2012;166(6):1221–9.
267. Omori K, Ohira T, Uchida Y, Ayilavarapu S, Batista EL, Yagi M,
Iwata T, Liu H, Hasturk H, Kantarci A.Priming of neutrophil oxidative burst in diabetes requires preassembly of the NADPH oxidase. J Leucocyte Biol. 2008;84(1):292–301.
268. Ruiz HH, Ramasamy R, Schmidt AM.Advanced glycation end
products: building on the concept of the “common soil” in metabolic disease. Endocrinology. 2020;161(1):bqz006.
269. Mao Q-Y, He S-Y, Hu Q-Y, Lu Y, Niu Y-X, Li X-Y, Zhang H-M,
Qin L, Su Q. Advanced glycation end products (AGEs) inhibit
macrophage efferocytosis of apoptotic β cells through binding to
the receptor for AGEs. J Immunol. 2022;208(5):1204–13.
270. van Zoelen MA, Schouten M, de Vos AF, Florquin S, Meijers J,
Nawroth PP, Bierhaus A, van der Poll T.The receptor for advanced
glycation end products impairs host defense in pneumococcal
pneumonia. J Immunol. 2009;182(7):4349–56.
271. Collison KS, Parhar RS, Saleh SS, Meyer BF, Kwaasi AA,
Hammami MM, Schmidt AM, Stern DM, Al-Mohanna FA.RAGEmediated neutrophil dysfunction is evoked by advanced glycation
end products (AGEs). J Leukoc Biol. 2002;71(3):433–44.
272. Zerr KJ, Furnary AP, Grunkemeier GL, Bookin S, Kanhere V, Starr
A.Glucose control lowers the risk of wound infection in diabetics
after open heart operations. Ann Thorac Surg. 1997;63(2):356–61.
273. Rayeld EJ, Ault MJ, Keusch GT, Brothers MJ, Nechemias C,
Smith H.Infection and diabetes: the case for glucose control. Am
J Med. 1982;72(3):439–50.
274. Golden SH, Peart-Vigilance C, Kao W, Brancati FL.Perioperative
glycemic control and the risk of infectious complications in a
cohort of adults with diabetes. Diabetes Care. 1999;22(9):1408–14.
275. Ata A, Lee J, Bestle SL, Desemone J, Stain SC.Postoperative
hyperglycemia and surgical site infection in general surgery
patients. Arch Surg. 2010;145(9):858–64.
276. Hotamisligil GS, Arner P, Caro JF, Atkinson RL, Spiegelman
BM.Increased adipose tissue expression of tumor necrosis factoralpha in human obesity and insulin resistance. J Clin Invest.
1995;95(5):2409–15.
277. Yaghini N, Mahmoodi M, Asadikaram GR, Hassanshahi GH,
Khoramdelazad H, Kazemi Arababadi M.Serum levels of interleukin 10 (IL-10) in patients with type 2 diabetes. Iran Red
Crescent Med J. 2011;13(10):752.
278. Everett E, Mathioudakis N.Update on management of diabetic
foot ulcers. Ann N Y Acad Sci. 2018;1411(1):153–65.
279. Dauwe PB, Pulikkottil BJ, Lavery L, Stuzin JM, Rohrich
RJ. Does hyperbaric oxygen therapy work in facilitating acute
wound healing: a systematic review. Plast Reconstr Surg.
2014;133(2):208e–15e.
280. Ramirez-Acuña JM, Cardenas-Cadena SA, Marquez-Salas PA,
Garza-Veloz I, Perez-Favila A, Cid-Baez MA, Flores-Morales
V, Martinez-Fierro ML. Diabetic foot ulcers: current advances
in antimicrobial therapies and emerging treatments. Antibiotics.
2019;8(4):193.
281. Perez-Favila A, Martinez-Fierro ML, Rodriguez-Lazalde JG, CidBaez MA, Zamudio-Osuna MJ, Martinez-Blanco M, MollinedoMontaño FE, Rodriguez-Sanchez IP, Castañeda-Miranda R,
Garza-Veloz I. Current therapeutic strategies in diabetic foot
ulcers. Medicina. 2019;55(11):714.
282. Golinko MS, Joffe R, Maggi J, Cox D, Chandrasekaran EB,
Tomic-Canic RM, Brem H. Operative debridement of diabetic
foot ulcers. J Am Coll Surg. 2008;207(6):e1–6.
283. Lebrun E, Tomic-Canic M, Kirsner RS. The role of surgical
debridement in healing of diabetic foot ulcers. Wound Repair
Regen. 2010;18(5):433–8.
284. Cardinal M, Eisenbud DE, Armstrong DG, Zelen C, Driver V,
Attinger C, Phillips T, Harding K.Serial surgical debridement: a
retrospective study on clinical outcomes in chronic lower extremity wounds. Wound Repair Regen. 2009;17(3):306–11.
285. Goldman MP, Clark CJ, Craven TE, Davis RP, Williams TK,
Velazquez-Ramirez G, Hurie JB, Edwards MS.Effect of intensive
glycemic control on risk of lower extremity amputation. J Am Coll
Surg. 2018;227(6):596–604.
286. Dronge AS, Perkal MF, Kancir S, Concato J, Aslan M, Rosenthal
RA. Long-term glycemic control and postoperative infectious
complications. Arch Surg. 2006;141(4):375–80.
287. Hanazaki K, Maeda H, Okabayashi T.Relationship between perioperative glycemic control and postoperative infections. World J
Gastroenterol. 2009;15(33):4122.
288. Lin J, Huang T, Wei H, Bao B, Gao T, Zheng X, Zhu H.Does
preoperative glycemic control restore immune defense against
implant-related infection in mice with diabetes? Clin Orthop Relat
Res. 2022;480(5):1008–17.
289. Åstrand A, Wingren C, Benjamin A, Tregoning JS, Garnett
JP, Groves H, Gill S, Orogo-Wenn M, Lundqvist AJ, Walters
D. Dapagliozin-lowered blood glucose reduces respiratory
Pseudomonas aeruginosa infection in diabetic mice. Br J
Pharmacol. 2017;174(9):836–47.
290. Howell-Jones RS, Wilson MJ, Hill KE, Howard AJ, Price PE,
Thomas DW. A review of the microbiology, antibiotic usage
and resistance in chronic skin wounds. J Antimicrob Chemother.
2005;55(2):143–9.
291. Abbas M, Uckay I, Lipsky BA.In diabetic foot infections antibiotics are to treat infection, not to heal wounds. Expert Opin
Pharmacother. 2015;16(6):821–32.
292. Armstrong DG, Lavery LA, Nixon BP, Boulton AJ. It’s not
what you put on, but what you take off: techniques for debrid-
17 Infection inDiabetes: Epidemiology, Immune Dysfunctions, andTherapeutics
https://t.me/med1917
325
ing and off-loading the diabetic foot wound. Clin Infect Dis.
2004;39(Suppl_2):S92–9.
293. Manna B, Nahirniak P, Morrison CA. Wound debridement.
Treasure Island, FL: StatPearls Publishing; 2022.
294. Lavery LA, Armstrong DG, Peters EJ, Lipsky BA.Probe-to-bone
test for diagnosing diabetic foot osteomyelitis: reliable or relic?
Diabetes Care. 2007;30(2):270–4.
295. Schaper NC, van Netten JJ, Apelqvist J, Bus SA, Hinchliffe RJ,
Lipsky BA, Board IE.Practical guidelines on the prevention and
management of diabetic foot disease (IWGDF 2019 update).
Diabetes Metab Res Rev. 2020;36:e3266.
296. Grill MF, Maganti RK. Neurotoxic effects associated with antibiotic use: management considerations. Br J Clin Pharmacol.
2011;72(3):381–93.
297. Singh R, Sripada L, Singh R.Side effects of antibiotics during
bacterial infection: mitochondria, the main target in host cell.
Mitochondrion. 2014;16:50–4.
298. James A, Larson T.Acute renal failure after high-dose antibiotic
bone cement: case report and review of the literature. Ren Fail.
2015;37(6):1061–6.
299. Balch A, Wendelboe AM, Vesely SK, Bratzler DW.Antibiotic prophylaxis for surgical site infections as a risk factor for infection
with Clostridium difcile. PLoS One. 2017;12(6):e0179117.
300. Poeran J, Mazumdar M, Rasul R, Meyer J, Sacks HS, Koll BS,
Wallach FR, Moskowitz A, Gelijns AC.Antibiotic prophylaxis and
risk of Clostridium difcile infection after coronary artery bypass
graft surgery. J Thorac Cardiovasc Surg. 2016;151(2):589–597.e2.
301. Lefer DA, Lamont JT.Clostridium difcile infection. N Engl J
Med. 2015;372(16):1539–48.
302. Zimlichman E, Henderson D, Tamir O, Franz C, Song P, Yamin
CK, Keohane C, Denham CR, Bates DW.Health care–associated
infections: a meta-analysis of costs and nancial impact on the US
health care system. JAMA Intern Med. 2013;173(22):2039–46.
303. McHugh S, Collins C, Corrigan M, Hill A, Humphreys H.The role
of topical antibiotics used as prophylaxis in surgical site infection
prevention. J Antimicrob Chemother. 2011;66(4):693–701.
304. Olid AS, Solà I, Barajas-Nava LA, Gianneo OD, Cosp XB, Lipsky
BA. Systemic antibiotics for treating diabetic foot infections.
Cochrane Database Syst Rev. 2015;(9):CD009061.
305. Faure E, Kwong K, Nguyen D. Pseudomonas aeruginosa in
chronic lung infections: how to adapt within the host? Front
Immunol. 2018;9:2416.
306. Ghotaslou R, Memar MY, Alizadeh N.Classication, microbiology and treatment of diabetic foot infections. J Wound Care.
2018;27(7):434–41.
307. Percival SL, Thomas J, Linton S, Okel T, Corum L, Slone W.The
antimicrobial efcacy of silver on antibiotic-resistant bacteria isolated from burn wounds. Int Wound J. 2012;9(5):488–93.
308. Choudhury H, Pandey M, Lim YQ, Low CY, Lee CT, Marilyn
TCL, Loh HS, Lim YP, Lee CF, Bhattamishra SK.Silver nanoparticles: advanced and promising technology in diabetic wound
therapy. Mater Sci Eng C. 2020;112:110925.
309. Liu X, Lee Py, Ho Cm, Lui VC, Chen Y, Che Cm, Tam PK,
Wong KK. Silver nanoparticles mediate differential responses
in keratinocytes and broblasts during skin wound healing.
ChemMedChem. 2010;5(3):468–75.
310. Nqakala ZB, Sibuyi NR, Fadaka AO, Meyer M, Onani MO,
Madiehe AM.Advances in nanotechnology towards development
of silver nanoparticle-based wound-healing agents. Int J Mol Sci.
2021;22(20):11272.
311. Al-Waili N, Salom K, Al-Ghamdi A, Ansari MJ.Antibiotic, pesticide, and microbial contaminants of honey: human health hazards.
Sci World J. 2012;2012:1.
312. Tibbles PM, Edelsberg JS.Hyperbaric-oxygen therapy. N Engl J
Med. 1996;334(25):1642–8.
313. Memar MY, Yekani M, Alizadeh N, Baghi HB.Hyperbaric oxygen therapy: antimicrobial mechanisms and clinical application
for infections. Biomed Pharmacother. 2019;109:440–7.
314. Elraiyah T, Tsapas A, Prutsky G, Domecq JP, Hasan R, Firwana
B, Nabhan M, Prokop L, Hingorani A, Claus PL.A systematic
review and meta-analysis of adjunctive therapies in diabetic foot
ulcers. J Vasc Surg. 2016;63(2):46S–58S.e2.
315. Chen C-E, Ko J-Y, Fong C-Y, Juhn R-J. Treatment of diabetic
foot infection with hyperbaric oxygen therapy. Foot Ankle Surg.
2010;16(2):91–5.
316. Kranke P, Bennett MH, Martyn-St James M, Schnabel A, Debus
SE, Weibel S. Hyperbaric oxygen therapy for chronic wounds.
Cochrane Database Syst Rev. 2015;(6):CD004123.
317. Tian X, Liang X, Song G, Zhao Y, Yang X.Maggot debridement
therapy for the treatment of diabetic foot ulcers: a meta-analysis. J
Wound Care. 2013;22(9):462–9.
318. Yoshida T, Aonuma H, Otsuka S, Ichimura H, Saiki E, Hashimoto
K, Ote M, Matsumoto S, Iwadate K, Miyawaki T.A human tissuebased assay identies a novel carrion blowy strain for maggot
debridement therapy. Sci Rep. 2022;12(1):12191.
319. Moya-López J, Costela-Ruiz V, García-Recio E, Sherman RA, De
Luna-Bertos E.Advantages of maggot debridement therapy for
chronic wounds: a bibliographic review. Adv Skin Wound Care.
2020;33(10):515–25.
320. Arabloo J, Grey S, Mobinizadeh M, Olyaeemanesh A,
Hamouzadeh P, Khamisabadi K. Safety, effectiveness and economic aspects of maggot debridement therapy for wound healing.
Med J Islam Repub Iran. 2016;30:319.
321. Parizad N, Hajimohammadi K, Goli R, Mohammadpour Y, Faraji
N, Makhdomi K. Surgical debridement and maggot debridement therapy (MDT) bring the light of hope to patients with
diabetic foot ulcers (DFUs): a case report. Int J Surg Case Rep.
2022;99:107723.
322. Mumcuoglu K, Davidson E, Avidan A, Gilead L.Pain related to
maggot debridement therapy. J Wound Care. 2012;21(8):400–5.
323. Khansa I, Schoenbrunner AR, Kraft CT, Janis JE.Silver in wound
care—friend or foe?: a comprehensive review. Plast Reconstr Surg
Glob Open. 2019;7(8):e2390.
324. Di Domenico EG, De Angelis B, Cavallo I, Sivori F, Orlandi F,
D’Autilio MFLM, Di Segni C, Gentile P, Scioli MG, Orlandi
A.Silver sulfadiazine eradicates antibiotic-tolerant Staphylococcus
aureus and Pseudomonas aeruginosa biolms in patients with
infected diabetic foot ulcers. J Clin Med. 2020;9(12):3807.
325. Bergin S, Wraight P. Silver based wound dressings and topical
agents for treating diabetic foot ulcers. Cochrane Database Syst
Rev. 2006;(1):CD005082.
326. Lansdown AB. Silver in health care: antimicrobial effects and
safety in use. Curr Probl Dermatol. 2006;33:17–34.
327. Wieman TJ, Smiell JM, Su Y.Efcacy and safely of a topical gel
formulation of recombinant human platelet-derived growth factor BB (becaplermin) in patients with chronic neuropathic diabetic
ulcers: a phase III randomized placebo-controlled double-blind
study. Diabetes Care. 1998;21(5):822–7.
328. Embil JM, Papp K, Sibbald G, Tousignant J, Smiell JM, Wong
B, Lau CY, C.B.S.Group. Recombinant human platelet-derived
growth factor-BB (becaplermin) for healing chronic lower extremity diabetic ulcers: an open-label clinical evaluation of efcacy.
Wound Repair Regen. 2000;8(3):162–8.
329. Gilligan AM, Waycaster CR, Milne CT. Cost effectiveness of becaplermin gel on wound closure for the treatment of pressure injuries. Wounds Compend Clin Res Pract.
2018;30(6):197–204.
330. Papanas D, Maltezos E.Benet-risk assessment of becaplermin in
the treatment of diabetic foot ulcers. Drug Saf. 2010;33(6):455–61.
Соседние файлы в папке Библиотека им академика М.И. Перельмана