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_531_Библиотеки_им_академика_М_И_Перельмана
.pdf
structure. LfcinB has been tested on neuroblastoma growth in vivo; nude rats carrying SH-
SY-5Y xenografts were given injections of 1.0 or 2.0 mg LfcinB; these rats’ cancer was signi-
cantly inhibited after LfcinB treatment, compared with untreated controls [176]. Anti-microbial
peptides can activate specic innate immune responses and immunomodulatory eects in the
host, even if the host is at risk or has been damaged. Furthermore, researchers have proposed
that anti-microbial peptides can modulate the host’s immune system through inammatory
responses and can stimulate benecial inammation; anti-microbial peptides might be able to
inhibit tumour growth.
9. Conclusion
From the injury to the wound recovery, there are a series of physiological responses that occur
in relation to immune cells. Polarisation of the macrophage is an important response in wound
healing. A series of inammatory factors are cited having notable function in the dierentiation
from novel macrophage into the classical macrophage (M1). The cellular mechanism involved
in the regulation of classical macrophage (M1) and alternative macrophage (M2) was docu-
mented in the wound healing process. At the present time, the M1/M2 dierentiation was
studied for selected immune responses. However, future studies may allow possible thera-
peutic targets considering this process in wound healing.
The immunotherapy that is being developed oers some advantageous immunomodulation
factors that are known in the eld of alternative medicine, such as mushroom beta-glucan,
anti-microbial peptides and triterpenoid; these factors represent a novel therapeutic approach
for anti-inammation. These factors may be a viable alternative approach to the problem of
drug resistance. Recent insights into wound healing and anti-inammation are promising;
however, exploiting these insights is complex because it involves chemistry, biology, instru-
mentation science and formulation science. Discovering new methods that are more eective
in targets is dicult. Immunotherapy might be an alternative therapy that can be applied in
the early phases of clinical therapy. Similarly, immunomodulation might be applicable in the
early phases of immune disease.
Author details
Yu-Sheng Wu1, Fan-Hua Nan2, Sherwin Chen1 and Shiu-Nan Chen
1*
*Address all correspondence to: d97b45004@ntu.edu.tw; snchen@ntu.edu.tw
1 College of Life Science, National Taiwan University, Taipei, Taiwan
2 Department of Aquaculture, National Taiwan Ocean University, Keelung, Taiwan
Polarisation of Macrophage and Immunotherapy in the Wound Healing
http://dx.doi.org/10.5772/63478
183
[1] P. Allavena, A. Sica, G. Solinas et al., “The inammatory micro-environment in tumor
progression: the role of tumor-associated macrophages,” Critical Reviews in Oncology/
Hematology, vol. 66, no. 1, pp. 1–9, 2008.
[2] S. S. Choe, K. C. Shin, S. Ka et al., “Macrophage HIF-2alpha ameliorates adipose tissue
inammation and insulin resistance in obesity,” Diabetes, vol. 63, no. 10, pp. 3359–71,
2014.
[3] Y. Enoki, T. Sato, S. Tanaka et al., “Netrin-4 derived from murine vascular endothelial
cells inhibits osteoclast dierentiation in vitro and prevents bone loss in vivo,” FEBS
Leers, vol. 588, no. 14, pp. 2262–9, 2014.
[4] B. Gore, M. Izikki, O. Mercier et al., “Key role of the endothelial TGF-beta/ALK1/
endoglin signaling pathway in humans and rodents pulmonary hypertension,” PLoS
One, vol. 9, no. 6, p. e100310, 2014.
[5] G. Poschmann, M. Grzendowski, A. Stefanski et al., “Redox proteomics reveal stress
responsive proteins linking peroxiredoxin-1 status in glioma to chemosensitivity and
oxidative stress,” Biochimica et Biophysica Acta, 2014.
[6] L. Wu, H. Chen, C. Curtis et al., “Go in for the kill,” Virulence, vol. 5, no. 7, pp. 710–21,
2014.
[7] J. H. Yu, and H. Kim, “Oxidative stress and inammatory signaling in cerulein
pancreatitis,” World Journal of Gastroenterology, vol. 20, no. 46, pp. 17324–9, 2014.
[8] E. Y. Choi, H. J. Kim, and J. S. Han, “Anti-inammatory eects of calcium citrate in RAW
264.7cells via suppression of NF-kappaB activation,” Environmental Toxicology and
Pharmacology, vol. 39, no. 1, pp. 27–34, 2014.
[9] C. S. Luo, J. R. Liang, Q. Lin et al., “Cellular responses associated with ROS production
and cell fate decision in early stress response to iron limitation in the diatom Thalassio‐
sira pseudonana,” Journal of Proteome Research, vol. 13, no. 12, pp. 5510–23, 2014.
[10] E. McNeill, M. J. Crabtree, N. Sahgal et al., “Regulation of iNOS function and cellular
redox state by macrophage Gch1 reveals specic requirements for tetrahydrobiopterin
in NRF2 activation,” Free Radical Biology & Medicine, vol. 79C, pp. 206–16, 2014.
[11] K. A. Redgrove, and E. A. McLaughlin, “The role of the immune response in Chlamydia
trachomatis infection of the male genital tract: a double-edged sword,” Frontiers in
Immunology, vol. 5, p. 534, 2014.
[12] F. Morescalchi, S. Duse, E. Gambicorti et al., “Proliferative vitreoretinopathy after eye
injuries: an overexpression of growth factors and cytokines leading to a retinal keloid,”
Mediators Inammation, vol. 2013, p. 269787, 2013.
Wound Healing: New insights into Ancient Challenges184
bial-triggered inammation and cancer,” Cellular Signalling, vol. 25, no. 2, pp. 403–16,
2013.
current views,” Ginekologia Polska, vol. 84, no. 4, pp. 293–7, 2013.
of adipose derived stromal cells promote alignment, organization, and maturation
of cardiomyocytes in vitro,” Journal of Biomedical Materials Research Part A, ,
2014.
pancreatic cancer,” Cancer Leers, vol. 345, no. 2, pp. 157–63, 2014.
progression and metastasis,” Oncoimmunology, vol. 1, no. 3, pp. 403–4, 2012.
through repression of PDGF receptor-alpha. Focus on ““Repression of PDGF-R-alpha
after cellular injury involves TNF-alpha, formation of a c-Fos-YY1 complex, and
302, no. 11, p. C1588–9, 2012.
Results in Cancer Research, vol. 180, pp. 103–14, 2010.
remodeling following infarction,” Molecular and Cellular Biochemistry, vol. 397, no. 1–2,
pp. 295–304, 2014.
late the production of MUC5AC mucin and probrotic cytokines involved in airway
tissue remodeling,” American Journal of Rhinology & Allergy, vol. 28, no. 2, pp. 103–9, –
2014.
vascularization of tissue engineering scaolds,” Biomaterials, vol. 35, no. 15, pp. 4477–
88, 2014.
transduction,” Annual Review of Plant Biology, vol. 55, pp. 373–99, 2004.
Biological Chemistry, vol. 383, no. 3–4, pp. 443–56, 2002.
reactive oxygen species,” Biochemistry (Moscow), vol. 70, no. 2, pp. 200–14, 2005.
Polarisation of Macrophage and Immunotherapy in the Wound Healing
http://dx.doi.org/10.5772/63478
185
therapy for inammatory diseases and cancers,” Journal of Hematology & Oncology, vol.
6, pp. 19, 2013.
oxidase-mediated signaling: potential roles in tissue repair, regenerative medicine and
tissue engineering,” Pharmacology & Therapeutics, vol. 122, no. 2, pp. 97–108, 2009.
in cellular stress response, stress tolerance, and tissue repair,” Pharmacolical Reviews,
vol. 63, no. 1, pp. 218–42, 2011.
wound healing in liver of nsh,” Fish and Shellsh Immunology, vol. 40, no. 1, pp. 174–
81, 2014.
ogy, vol. 552, no. Pt 2, pp. 335–44, 2003.
required for directional migration of resident and bone marrow-derived hepatic pro-
brogenic cells,” Journal of Hepatology, vol. 54, no. 5, pp. 964–74, 2011.
the migration of monocytes across the blood-brain barrier in vitro,” FASEB Journal, vol.
15, no. 10, pp. 1852–4, 2001.
and cellular consequences,” Science, vol. 268, no. 5208, pp. 239–47, 1995.
apoptosis link,” Nature Reviews Molecular Cell Biology, vol. 4, no. 7, pp. 552–65, 2003.
and energy charge in cultured endothelial and P388D1 cells after oxidant injury,”
Journal of Clinical Investigation, vol. 76, no. 4, pp. 1471–6, 1985.
artery and aortic endothelial cells to reactive oxygen products,” American Journal of
Respiratory Cell and Molecular Biology, vol. 4, no. 1, pp. 4–10, 1991.
canine vessels induces ICAM-1 and CD18-dependent neutrophil adherence,” Circula‐
tion, vol. 84, no. 5, pp. 2154–66, 1991.
induced increase in endothelial permeability,” American Journal of Physiology–Lung
Cellular and Molecular Physiology, vol. 14, no. 6, pp. L973, 1996.
Wound Healing: New insights into Ancient Challenges186
istry, vol. 287, no. 7, pp. 4434–40, 2012.
Frontiers in Pharmacology, vol. 5, 2014.
resident macrophages,” Immunological Reviews, vol. 262, no. 1, pp. 25–35, 2014.
and pericytes: a review of function and identication,” Journal of Leukocyte Biology, vol.
75, no. 3, pp. 388–97, 2004.
liver homeostasis and pathology,” Hepatology, vol. 59, no. 5, pp. 2034–42, 2014.
suppress while recruited macrophages promote allergic lung inammation in murine
models of asthma,” American Journal of Respiratory and Critical Care Medicine, vol. 189,
pp. A3685, 2014.
cardiac macrophages are maintained through distinct mechanisms at steady state and
during inammation,” Immunity, vol. 40, no. 1, pp. 91–104, 2014.
Myb and hematopoietic stem cells,” Science, vol. 336, no. 6077, pp. 86–90, 2012.
and endothelial cells in regenerating rat liver. A light and electron microscopic
cytochemical study,” The American Journal of Pathology, vol. 80, no. 3, pp. 349, 1975.
tumor-associated macrophages in the Lewis lung carcinoma,” BioMed Research Inter‐
national, 2014.
immunologic functional perspective,” Annual Review of Immunology, vol. 27, pp. 451–
83, 2009.
tumour environment by TGFβ,” Nature Reviews Immunology, vol. 10, no. 8, pp. 554–67,
2010.
The Journal of Clinical Investigation, vol. 122, no. 3, pp. 787–95, 2012.
zation in tissue repair and remodelling,” The Journal of Pathology, vol. 229, no. 2, pp.
176–85, 2013.
Polarisation of Macrophage and Immunotherapy in the Wound Healing
http://dx.doi.org/10.5772/63478
187
polarization,” Frontiers in Bioscience: A Journal and Virtual Library, vol. 13, pp.
453–61, 2007.
macrophages as a paradigm for polarized M2 mononuclear phagocytes,” Trends in
Immunology, vol. 23, no. 11, pp. 549–55, 2002.
Agaricus brasiliensis (1→6)-β-d-glucans show immunostimulatory activity on human
THP-1 derived macrophages,” Carbohydrate Polymers, vol. 94, no. 1, pp. 91–9,
2013.
peripheral endogenous opioid-mediated analgesia in inammation,” Molecular Pain,
vol. 10, no. 1, pp. 10, 2014.
alternative activation of adipose tissue macrophages,” Diabetes, vol. 61, no. 11, pp. 2718–
27, 2012.
M1–M2 polarization balance,” Frontiers in Immunology, vol. 5, 2014.
is a key determinant of dierential macrophage activation and function,” Journal of
Leukocyte Biology, vol. 90, no. 5, pp. 845–54, 2011.
functions,” Immunity, vol. 32, no. 5, pp. 593–604, 2010.
extracellular double-stranded RNA to mediate cellular inammatory responses,” The
Journal of Immunology, vol. 190, no. 1, pp. 115–25, 2013.
M2 polarization concept. Part I. Proinammatory phenotype,” Biochemistry (Moscow),
vol. 77, no. 3, pp. 246–60, 2012.
of IRF4 via the NFAT pathway leads to IL-10 expression in B cells,” PLoS Pathogens, vol.
10, no. 1, pp. e1003858, 2014.
phage polarization and Th1/Th17 response,” Nature Immunology, 2011.
IRF8 to promote inammatory macrophage polarization,” Nature Immunology, vol. 13,
no. 7, pp. 642–50, 2012.
Wound Healing: New insights into Ancient Challenges188
duction and loss of mitochondrial transmembrane potential during hepatic cell death
induced by LPS/d-GalN,” Journal of Molecular Biology, vol. 369, no. 4, pp. 967–84, 2007.
macrophage programming in mice by Lyn/Hck, SHIP, and Stat5,” The Journal of Clinical
Investigation, vol. 118, no. 3, pp. 924, 2008.
polarization in adipose tissue and improves systemic glucose tolerance via interleu-
kin-4 (IL-4)/STAT6 protein signaling axis in obesity,” Journal of Biological Chemistry, vol.
287, no. 17, pp. 13561–71, 2012.
apoptosis: a protective mechanism against alcoholic and nonalcoholic fay liver
disease,” Hepatology, vol. 59, no. 1, pp. 130–42, 2014.
induced by prostaglandin E2 and IL-6 from cervical carcinoma are switched to activated
M1 macrophages by CD4+ Th1 cells,” The Journal of Immunology, vol. 187, no. 3, pp.
1157–65, 2011.
on the evolving roles of coordinated regulation of cellular signaling pathways,” Cellular
Signalling, vol. 26, no. 2, pp. 192–7, 2014.
Cell Metabolism, vol. 19, no. 6, pp. 898–9, 2014.
advanced glycation end products to prevent formation of abdominal aortic aneurysm
in a murine model,” Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 34, no. Suppl
1, p. A114, 2014.
in a metastatic melanoma model in the mouse,” Cancer Research, vol. 72, no. 8 Suppl,
pp. 402, 2012.
cytokines to facilitate the M1-to-M2 transition of macrophages and enhance vasculari-
zation of bone scaolds,” Biomaterials, vol. 37, pp. 194–207, 2015.
inammatory M1 macrophages by microRNA-155,” Journal of Molecular Cell Biology,
vol. 4, no. 5, pp. 341–3, 2012.
proliferation through IL-10–dependent M2 polarization of tumor-associated macro-
phages,” Cancer Research, vol. 73, no. 12, pp. 3604–14, 2013.
Polarisation of Macrophage and Immunotherapy in the Wound Healing
http://dx.doi.org/10.5772/63478
189
disease,” Nature Reviews Immunology, vol. 11, no. 2, pp. 85–97, 2011.
disease,” Cell Metabolism, vol. 13, no. 1, pp. 11–22, 2011.
serpinopathies,” The Journal of Experimental Medicine, vol. 205, no. 7, pp. 1529–34, 2008.
polymerization of mutant neuroserpin,” Nature, vol. 401, no. 6751, pp. 376–9, 1999.
England Journal of Medicine, vol. 352, no. 16, pp. 1685–95, 2005.
Neurobiology of Aging, vol. 21, no. 3, pp. 383–421, 2000.
homeostasis and disease,” Nature, vol. 496, no. 7446, pp. 445–55, 2013.
Journal of Clinical Investigation, vol. 122, no. 3, pp. 787–95, 2012.
intestinal dendritic cell and macrophage subsets that control Th17 and regulatory T cell
responses are dependent on the T cell/APC ratio, source of mouse strain, and regional
localization,” The Journal of Immunology, vol. 187, no. 2, pp. 733–47, 2011.
Reviews Cancer, vol. 9, pp. 239–52, 2009.
2002.
implications. Springer, 2009.
microenvironment,” Frontiers in Bioscience (Landmark Ed), vol. 15, pp. 166–79, 2010.
chronic inammation to cancer,” Clinical Immunology, vol. 134, pp. 237–50, 2010.
and disease. Garland Science, 2005.
peutic relevance,” Nature Reviews Cancer, vol. 5, pp. 263–74, 2005.
Wound Healing: New insights into Ancient Challenges190
[95] G. P. Dunn, A. T. Bruce, H. Ikeda et al., “Cancer immunoediting: from immunosurveil-
lance to tumor escape,” Nature Immunology, vol. 3, pp. 991–8, 2002.
[96] G. P. Dunn, L. J. Old, and R. D. Schreiber, “The immunobiology of cancer immunosur-
veillance and immunoediting,” Immunity, vol. 21, pp. 137–48, 2004.
[97] B. Z. Qian, and J. W. Pollard, “Macrophage diversity enhances tumor progression and
metastasis,” Cell, vol. 141, pp. 39–51, 2010.
[98] D. W. Siemann, “Tumor microenvironment. Wiley Online Library, 2011.
[99] N. Mach, S. Gillessen, S. B. Wilson et al., “Dierences in dendritic cells stimulated in
vivo by tumors engineered to secrete granulocyte-macrophage colony-stimulating
factor of t3-ligand,” Cancer Research, vol. 60, pp. 3239–46, 2000.
[100] S. K. Biswas, and A. Mantovani, “Macrophage plasticity and interaction with lympho-
cyte subsets: cancer as a paradigm,” Nature Immunology, vol. 11, pp. 889–96, 2010.
[101] B. Ruell, N. I. Aara, and L. M. Coussens, “Dierential macrophage programming in
the tumor microenvironment,” Trends in Immunology, vol. 33, pp. 119–126, 2012.
[102] R. A. Flavell, S. Sanjabi, S. H. Wrzesinski et al., “The polarization of immune cells in the
tumour environment by TGFbeta,” Nature Reviews Immunology, vol. 10, pp. 554–67,
2010.
[103] L. Bingle, N. J. Brown, and C. E. Lewis, “The role of tumour-associated macrophages
in tumour progression: implications for new anticancer therapies,” The Journal of
Pathology, vol. 196, pp. 254–65, 2002.
[104] J. W. Pollard, “Tumour-educated macrophages promote tumour progression and
metastasis,” Nature Reviews Cancer, vol. 4, pp. 71–78, 2004.
[105] A. Mantovani, A. Sica, S. Sozzani et al., “The chemokine system in diverse forms of
macrophage activation and polarization,” Trends in Immunology, vol. 25, pp. 677–86,
2004.
[106] A. Mantovani, and A. Sica, “Macrophages, innate immunity and cancer: balance,
tolerance, and diversity,” Current Opinion in Immunology, vol. 22, pp. 231–7, 2010.
[107] A. Mantovani, A. Sica, P. Allavena et al., “Tumor-associated macrophages and the
related myeloid-derived suppressor cells as a paradigm of the diversity of macrophage
activation,” Human Immunology, vol. 70, pp. 325–30, 2009.
[108] C. Steidl, T. Lee, S. P. Shah et al., “Tumor-associated macrophages and survival in classic
Hodgkin’s Lymphoma,” The New England Journal of Medicine, vol. 362, pp. 875–85, 2010.
[109] K. D. Elgert, D. G. Alleva, and D. W. Mullins, “Tumor-induced immune dysfunction:
the macrophage connection,” Journal of Leukocyte Biology, vol. 64, pp. 275–90, 1998.
[110] C. Sunderköer, M. Goebeler, K. Schulze-Ostho et al., “Macrophage-derived angio-
genesis factors,” Pharmacology & Therapeutics, vol. 51, pp. 195–216, 1991.
Polarisation of Macrophage and Immunotherapy in the Wound Healing
http://dx.doi.org/10.5772/63478
191
[111] E. Giraudo, M. Inoue, and D. Hanahan, “An amino-bisphosphonate targets MMP-9-
expressing macrophages and angiogenesis to impair cervical carcinogenesis,” The
Journal of Clinical Investigation, vol. 114, pp. 623–33, 2004.
[112] A. Ben-Baruch, “Inammation-associated immune suppression in cancer: the roles
played by cytokines, chemokines and additional mediators,” Seminars in Cancer
Biology, vol. 16, pp. 38–52, 2006.
[113] M. Mitsuhashi, J. Liu, S. Cao et al., “Regulation of interleukin-12 gene expression and
its anti-tumor activities by prostaglandin E2 derived from mammary carcinomas,”
Journal of Leukocyte Biology, vol. 76, pp. 322–32, 2004.
[114] A. Mantovani, S. Sozzani, M. Locati et al., “Macrophage polarization: tumor-associated
macrophages as a paradigm for polarized M2 mononuclear phagocytes,” Trends in
Immunology vol. 23, pp. 549–55, 2002.
[115] G. Solinas, G. Germano, A. Mantovani et al., “Tumor-associated macrophages (TAM)
as major players of the cancer-related inammation,” Journal of Leukocyte Biology, vol.
86, pp. 1065–73, 2009.
[116] M. P. Fink, “Role of reactive oxygen and nitrogen species in acute respiratory distress
syndrome,” Current Opinion in Critical Care, vol. 8, no. 1, pp. 6–11, 2002.
[117] F. Dong, X. C. Zhang, S. Y. Li et al., “Possible involvement of NADPH oxidase and JNK
in homocysteine-induced oxidative stress and apoptosis in human umbilical vein
endothelial cells,” Cardiovascular Toxicology, vol. 5, no. 1, pp. 9–20, 2005.
[118] E. Novo, C. Buslea, L. V. Bonzo et al., “Intracellular reactive oxygen species are
required for directional migration of resident and bone marrow-derived hepatic pro-
brogenic cells,” Journal of Hepatology, vol. 54, no. 5, pp. 964–74, 2011.
[119] A. Van der Goes, D. Wouters, S. M. Van Der Pol et al., “Reactive oxygen species enhance
the migration of monocytes across the blood-brain barrier in vitro,” FASEB Journal :
Ocial Publication of the Federation of American Societies for Experimental Biology, vol. 15,
no. 10, pp. 1852–4, 2001.
[120] J. W. Park, S. W. Ryter, and A. M. Choi, “Functional signicance of apoptosis in chronic
obstructive pulmonary disease,” COPD, vol. 4, no. 4, pp. 347–53, 2007.
[121] S. W. Ryter, H. P. Kim, A. Hoeel et al., “Mechanisms of cell death in oxidative stress,”
Antioxid Redox Signal, vol. 9, no. 1, pp. 49–89, 2007.
[122] M. L. Circu, and T. Y. Aw, “Reactive oxygen species, cellular redox systems, and
apoptosis,” Free Radical Biology and Medicine, vol. 48, no. 6, pp. 749–62, 2010.
[123] B. T. Mossman, “Introduction to serial reviews on the role of reactive oxygen and
nitrogen species (ROS/RNS) in lung injury and diseases,” Free Radical Biology and
Medicine, vol. 34, no. 9, pp. 1115–6, 2003.
Wound Healing: New insights into Ancient Challenges192
Соседние файлы в папке Библиотека им академика М.И. Перельмана