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Nutrition and Malnutrition in Inflammatory Bowel Disease 111
An excellent analysis of clinical trials suggested
that lipid composition may play a major role in the
effect of EN as primary care in Crohn’s disease [82].
High-lipid formulas, particularly linoleic acid formu-
las, were associated with worse results, whereas low-
lipid formulas and those with large amounts of
MUFA have yielded better results. Linoleic acid is the
precursor of arachidonic acid, which constitutes the
substrate for the synthesis of factors with a substan-
tial pro-inflammatory action (IL-6, LTB-4, PGE
2
,
thromboxane A
2
), the content of which is increased
in the active phases of Crohn’s disease. EN formulas
rich in n-6 PUFA such as linoleic acid, which is capa-
ble of inducing marked synthesis of arachidonic acid
and of pro-inflammatory factors, would be, there-
fore, less indicated than diets with a low content of
PUFA or containing PUFA of the n-3 series which
induces the synthesis of factors with a less pro-
nounced pro-inflammatory activity (LTB-5, PGE
3
and PGI
2
)—the synthesis of which competes with
that of the factors with stronger pro-inflammatory
action. Furthermore, this would also reduce the syn-
thesis of cytokines—tumour necrosis factor (TNF-
alfa) and platelet activating factor (PAF)—involved
in tissue-damaging mechanisms. Dietary n-3 PUFA
promoted an anti-inflammatory effect in experimen-
tal colitis, by affecting the immune cell function, by
reducing myeloid cell recruitment and activation of
myofibroblasts, pro-inflammatory cytokines, by
enhancing epithelial barrier function and by acting
on the tight junction and up-regulation of
occludines. The ratio n-6/n-3, more than their
absolute levels, with competition for COX and 5-
LOX, seems to determine the final eicosanoid balance
[85]. However, increased biosynthesis, consumption
of PUFA and high circulating levels of n-3 PUFA in
active Crohn’s have been described [86], raising
some doubts on the need for high n-3 content enter-
al formulas.
Bone Disease in IBD
Reduced bone mineral density (BMD) is frequently
associated with Crohn’s disease (CD). Early studies
have described a high prevalence of osteopenia (a T-
score of –1 or lower) and osteoporosis (a T-score of
–2.5 or lower) in inflammatory bowel disease (IBD).
Uncontrolled studies gave a prevalence of severe
demineralisation determined by dual-energy absorp-
tiometry (Z-score of lower than –2 or T-score of
lower than –2.5) that ranged from 18 to 42%, while
larger studies with a healthy control group showed
prevalence rates of only 2–16% [87]. It is important
to notice that these studies are prone to selection bias
as they are conducted in specialised IBD centres. In
fact, in prospective longitudinal studies, changes in
BMD in patients with IBD were similar to those of the
general population [88]. The most relevant clinical
question is to determine whether alterations in BMD
can affect the fracture risk. There have been four
large population-based studies describing fracture
risk in patients with IBD. A survey was mailed to
members of the Danish Crohn’s/Colitis Association
regarding fractures [89]. The authors concluded that
patients with UC had similar overall fracture rates
compared with control subjects. Crohn’s disease
patients had a relative risk of 1.7 for all fractures (RR
for female patients 2.5, 2.9 among premenopausal
females, 1.8 among postmenopausal women and 0.6
among men) compared to the control group. A fam-
ily fracture history (RR 2.4) especially paternal (RR
3.6) increased the risk of fracture among patients
with CD. Among UC patients, maternal fracture his-
tory (RR 2.4) and smoking (RR 3.8) were additional
risk factors. There was no correlation between frac-
ture risk and steroid use in both CD and UC. It is
important to notice that the control subjects were not
matched to patients by age and gender and were
more likely to be older and male, and less likely to be
current smokers or on hormone replacement therapy
than patients with Crohn’s disease. Furthermore,
there may have been a bias in the nature of patients
who returned the questionnaire, as those who were at
higher risk may have been more likely to respond. In
population-based studies, the same authors observed
that the relative risk of sustaining a fracture requir-
ing hospitalisation in CD was 1.9, whereas at 1.08 in
UC it had not significantly increased [90].
There have been two North American population-
based studies of fracture risk in IBD [91, 92]. The first
study, published by Bernstein et al., identified hospi-
tal and out-patient fractures by collecting the data via
administrative databases for the Canadian province
of Manitoba. The overall fracture rate for patients
with IBD was found to be approximately 1 per
100 patient-years and this increased to a relative risk
of 1.
41 compared with an age-gender- and geograph-
ical residence-matched control group. There was an
increased fracture risk of the hip and of the spine,
which was evidenced in patients over 60 years of age.
No differences were observed between men and
women and between CD and UC patients. However,
there was a significantly increased fracture risk for
UC male patients compared with females. The other
North American study used the Olmsted County
population-based database of 243 CD patients. Com-
pared with controls, the overall risk ratio for any
fracture was 0.9, whereas the relative risk for an
osteoporotic fracture was 1.4. The risk ratio for tho-
racolumbar vertebral fracture was 2.2. Thus, the risk
of fracture was not greater than in the general popu-
112 I. Vantini, F. De Iorio, N. Tacchella, L. Benini
lation, except in the elderly. The last study was a pri-
mary care-based nested-case control study which
used a General Practice Research Database in the UK
that included 683 patients [93]. The overall odds ratio
for IBD patients compared with a matched control
group was 1.21 without differences between males
and females. After accounting for a measure of dis-
ease severity, there were no significant differences in
the fracture risk between patients with CD and UC;
the risk of fracture correlated with the number of
symptoms and with age.
The collective messages of these studies are the
following: (1) patients with IBD may have increased
fracture rates but the magnitude of the excess risk is
small and most evident in the elderly; (2) fracture
risk is generally similar in CD and UC; (3) osteo-
porosis is gender neutral among patients with IBD.
Risk Factor for Osteoporosis in IBD
The mechanisms underlying bone loss in IBD are still
unclear. Several factors that also contribute to osteo-
porosis in the general population are implicated:
physical inactivity, hypogonadism, underweight, cal-
cium and vitamin D deficiency, malnutrition, smok-
ing (most commonly in CD), treatment with steroids
and the effects of inflammatory cytokines related to
the disease activity. As noted before, among patients
with IBD, fracture risk, which is similar in CD and
UC, is gender neutral and most evident in adults. In
the following, we will briefly discuss the other main
risk factors.
Onset of inflammatory bowel disease. A recent
analysis of premenopausal adult women with early
onset IBD did not provide evidence that an early
onset of disease is a major risk factor for early onset
osteoporosis [94].
Steroid use. Systemic steroid therapy is associated
with rapid bone loss, particularly in the trabecular
bone of the lumbar spine. Steroid use is a major fac-
tor in IBD-associated bone loss. Nevertheless, it is
difficult to separate the effects of corticosteroid use
from those of disease activity. Bernestein et al.
observed that corticosteroid use in the 2-year period
preceding fracture was more frequently in patients
experiencing fracture compared with those not expe-
riencing fractures [94]. Few studies have examined
BMD in newly diagnosed patients. Gosh et al.
observed reduced BMD in patients with CD, but not
with UC [95]. This could be explained by the relative
lower age and hence higher BMD of the UC patients
and by the high preponderance of proctitis with less
deleterious systemic consequences. BMD was unaf-
fected by the subsequent use of steroids over a 1-year
period. Schoon et al. [96] found BMD to be normal at
diagnosis. It has been suggested that the high preva-
lence of oral contraceptives used in this study (92%
of the women) may have provided protection against
bone loss. Lamb et al. [97] observed a reduced BMD
at diagnosis, prior to corticosteroid treatment in 34
IBD patients.
Calcium intake, vitamin D deficiency, malabsorp-
tion, intestinal resection, body mass index. Adequate
calcium-intake has been suggested as being an
important determinant of optimal bone mass. Bern-
stein et al. observed, in a cohort of premenopausal
women prior to 20 years of age, that the average BMD
was not different than in controls and only 3% had
BMD in the osteoporotic range [94]. Therefore, IBD
children achieve normal BMD as adults and it is pos-
sible that during remission periods or steroid-free
periods there is a sufficient opportunity to achieve
normal bone mineralisation. In this same study, oral
calcium and vitamin D intake were measured by a 4-
day food record and no correlation was observed
between the intake of these nutrients and BMD [98];
this is similar to a previous report in 168 CD patients
[99]. Hence, a 4-day record can be beneficial in deter-
mining the quantity of calcium supplementation
required. One variable often cited as being important
in CD is the relationship between osteomalacia, the
skeletal hallmark of vitamin D deficiency, and
reduced vitamin D intake and/or absorption. Factors
contributing to vitamin D deficiency in CD include
malabsorption of dietary vitamin D and 25-hydroxy
vitamin D undergoing enterohepatic circulation, lack
of adequate sun exposure, a low dietary vitamin D
intake and the ingestion of drugs interacting with the
intestinal absorption of vitamin D. The majority of
the studies suggest that low dietary intake of vitamin
D is not an important determinant of BMD in IBD
patients [100]. Cholestyramine is often used to con-
trol postresectional diarrhoea due to bile acid malab-
sorption. Both resection of the terminal ileum and
cholestyramine therapy lead to the depletion of bile
acids, which are essential for vitamin D absorption;
ensuring adequate intake of vitamin D is highly rec-
ommended especially in patients with small-bowel
resection. Most of the studies on the importance of
vitamin D deficiency come from literature in the
early 1980s that specifically addressed BMD in a
selected group of CD patients with decreased serum
25-OHD. A recent study showed that vitamin D
absorption in CD patients is normal [101]. Some
studies have shown no relationship between BMD
and measured serum 25-OHD [
102–104]. Two stud-
ies have found that serum 25-OHD levels are actually
lower in UC than in CD [105, 106]. Relative malnutri-
tion and low body weight are important risk factors.
In the general population, body mass index is strong-
ly correlated with BMD [107] and meta-analysis has
Nutrition and Malnutrition in Inflammatory Bowel Disease 113
concluded that a low body weight is a significant and
consistent risk factor for fracture in the general pop-
ulation, although the 51 studies used were dominat-
ed by older women [108]. The same appears true for
CD patients. In a population-based study of 60 CD
patients, 60 UC patients and 60 healthy controls,
those with CD had both a lower BMD as well as lower
lean mass [109]. This effect was only seen in those
with current or past systemic steroid use, which is
consistent with the known adverse drug effects on
both bone and muscle tissue. Among 168 CD
patients, the BMI was significantly correlated with
BMD (p<0.0001) [110].
Inflammation-mediated bone loss. The link
between inflammation and bone loss may be of par-
ticular interest in IBD-associated osteopenia. The
recently discovered receptor activator of nuclear fac-
tor κB (RANK) ligand (RANKL) osteoprotegerin
(OPG), may be the important link between systemic
inflammation and osteoporosis. The OPG molecule
binds to the receptor activator of nuclear factor κB
(RANK). The effect of this ligation is to regulate T
cell–dendritic cell communications, dendritic cell
survival and lymph node organogenesis. The interac-
tion of RANK on the surface of the osteoclasts with
its ligand RANKL induces osteoclastogenesis. Osteo-
protegerin (OPG) can be secreted by osteoblasts and
serves as a decoy receptor that prevents the ligation
of RANKL, which can interfere with osteoclastogene-
sis. The balance between RANKL and OPG is of
major importance for the regulation of osteoclasto-
genesis. The way in which compounds stimulate
RANK ligand or OPG will affect whether they inhibit
or induce osteoclastogenesis. Certain pro-inflamma-
tory cytokines such as IL-1 and TNF alfa, induce
RANKL and displace the balance of bone formation
and bone reabsorption in favour of bone reabsorp-
tion causing bone loss. Corticosteroids partially exert
their toxic effects on bone by the same mechanism
and they also inhibit OPG production.
Genetic risk factors of rapid bone loss. An interest-
ing report linked potential fracture risk as a measure
of bone mineral density by DXA with the presence or
absence of specific alleles for certain proinflammato-
ry cytokines [111]. Eighty-three patients with IBD
were enrolled and went through a follow-up with
BMD measurements over 1.6±0.3 years: 17% had a T-
score below –2.5 at the spine and 11% had a T-score
below –2.5 at the hip. They observed that the extent
of bone loss was not correlated to clinical severity of
disease or administration of steroids. Non-carriage
of the 240-base pair allele of the IL-1ra gene and car-
riage of the 130-base pair allele of IL-6 were inde-
pendently associated with increased bone loss, and
their combined presence was significantly associated
with increased bone loss. Todhunter et al. [112]
investigated the influence of IL-6, collagen type 1a1
(COL1A1 ) and vitamin D receptor gene (VDR) sin-
gle nucleotide polymorphisms (SNP) on BMD in a
cohort of 245 patient’s with CD. They observed that
lumbar spine and total hip BMD was higher in
patients with CC genotype compared to GG (p=
0.041
and p=0.014 respectively). In patients genotyped for
COL1A1, (hip, but not lumbar spine), BMD was high-
er in the homozygous wild type GG than in the het-
erozygous GT. No differences were observed either
between BMD VDR Taq 1 and Fok 1 genotypes or
between BMD and CARD 15 genotypes. The authors
observed that in CD, a condition characterised by
increased levels of IL-6, the genotype CC is protective
against IL-6 mediated bone reabsorption. Further-
more, COL1A1 gene polymorphisms at the Sp1 bind-
ing sites are thought to influence the properties of
bone by altering the level of transcription and pro-
duction of collagen. It has been observed that bone
strength is reduced in heterozygous compared to
wild type subjects [113].
Clinical Trials on Prevention and Therapy of IBD-Associated Bone
Disease
Therapeutic intervention studies focussing on IBD
are sparse and no clinical trials with the aim of frac-
ture prevention are available. Extrapolating results
from fracture prevention trials in osteoporotic and
steroid-induced osteoporosis may be tricky for sev-
eral reasons: (1) orally administered agents, especial-
ly biphosphonates whose absorption is only 1–5%
even in healthy subjects, may not be adequately
absorbed in those with intestinal disease (in patients
with active disease, especially of the upper gastroin-
testinal tract, parenteral administration of biphos-
phonates may be appropriate); (2) IBD is under-rep-
resented in the larger intervention trials on steroid-
induced osteoporosis, making the conclusions
arguable; (3) younger men and premenopausal
women—patients of special interest with regard to
IBD-associated bone disease—have not been subject-
ed to therapeutic intervention trials outside the con-
text of steroid-induced osteoporosis. Taking all these
drawbacks as a whole, review articles on the therapy
of IBD-associated bone disease should be considered
with caution. Experts emphasise lifestyle modifica-
tions (physical exercise, no smoking and alcohol
excess), vitamin D (400–800 IE daily) and calcium (1
000–1 500 mg/day) supplementation and hormone
replacement therapy (oestrogens or selective oestro-
gens receptor modulators in women; testosterone in
hypogonadal men). However, these recommenda-
tions are far from fully evaluated. The factors that are
known at the present are discussed in the following.
114 I. Vantini, F. De Iorio, N. Tacchella, L. Benini
Firstly, vitamin D supplementation is relatively
inexpensive and does not necessitate control of calci-
um levels at regular intervals. It should be considered
for all older patients (>60 years) because of the
known high prevalence of vitamin D deficiency. In
contrast, active vitamin D metabolites are expensive,
necessitate control of calcium serum levels and have
not been shown to be effective for fracture reduction.
Secondly, calcium supplementation does not appear
to be essential in patients who are being supplement-
ed with genuine vitamin D. In addition, calcium is
not well tolerated. Thirdly, early menopause or male
hypogonadism should be corrected with hormone
replacement therapy and fourthly, the dose of corti-
costeroids should be kept to a minimum and non-
systemic or controlled-release formulations should
be advised [114].
Previous short-term studies have indicated that
biphosphonates and slow release sodium fluoride
can improve BMD. No effects were seen after 1 year
in a randomised study of corticosteroid-using
patients with IBD with the administration of calcium
and vitamin D alone [115]. One small, randomised
placebo-controlled study of 32 CD patients addressed
the changes in BMD after a year-long therapy with
the oral bisphosphonate alendronate 10 mg/day
[116]. After one year, the bone mineral density had
increased significantly at the spine in the alen-
dronate-treated group compared with the control
group and showed a trend for recovery at the femoral
neck. However, several issues have to be considered
when interpreting the data of this study. First of all,
the patients were selected for disease quiescence, and
patients with active disease, whose bone microenvi-
ronment may be more exposed to bone-resorbing
cytokines or whose ability to absorb oral biphospho-
nates may be compromised, were excluded. Addi-
tionally, although the study was randomised, the
alendronate-treated group had significantly higher
levels of biochemical markers of bone reabsorption
at baseline, which may have improved the response
to anti-reabsorptive therapy. There are, however,
some encouraging aspects: the favourable response
of CD patients to oral and the good tolerability of the
drug in these patients. In a more recent randomised
controlled study, Von Tirpitz et al. randomised 84
CD patients with reduced BMD to receive calcium
citrate (800 mg/day plus vitamin D 1 000 IU/day)
alone (n=13) or with either slow release sodium fluo-
ride (25 mg twice daily; n=36) or ibandronate (1 mg
intravenously every 3 months; n=35) [117]. The ran-
domisation was unbalanced as patients with osteo-
porosis were assigned either to the fluoride group or
to the ibandronate group. Other problems were the
shorter average disease duration in the fluoride
group and incomplete follow-up. At 27 months, lum-
bar bone density increased by 2.6% (p=0.066) for the
group given only calcium and vitamin D, 5.7%
(p=0.003) for those given fluoride and 5.4%
(p=0.003) for those given ibandronate; this effect was
particularly evident during the first year. Femoral
BMD did not change in any group and no participant
suffered a new vertebral fracture. Thirty-five patients
who received steroids at least once during the study
showed a mean increase in BMD similar to that
observed in those who did not receive steroids. A sig-
nificant correlation was observed between BMI and
the BMD during the observational period and
improved nutrition may alone contribute to the
improvement of BMD (p<0.001), emphasising that
treatment of underlying bowel disease and associated
improvement of body weight may be important fac-
tors in the management of osteoporosis. Bernstein et
al. [118] measured the BMD in 46
CD patients treat-
ed with infliximab for 1 year. At baseline, reduced
BMD occurred in 43% of patients at the lumbar spine
and 46% at the left femur; after 1 year of therapy,
BMD was significantly increased. BMD gain between
the groups with and without osteopenia was not dif-
ferent. Changes in BMD were not correlated to con-
current steroid therapy, calcium supplementation or
changes in C-reactive proteins.
Conclusions
Malnutrition is rather frequent in Crohn’s disease,
particularly in children and in adults with unremit-
ting and/or complicated disease. Several factors can
contribute to malnutrition and some of them can be
shared by the same patient. Early and/or subtle nutri-
tional changes should be considered in the compre-
hensive evaluation of patients affected by IBD. Bone
changes and increased fracture risk have been
described in both Crohn’s disease and ulcerative coli-
tis. Though chronic use of steroids has been consid-
ered a determinant in BMD impairment, the rela-
tionship between steroid administration and fracture
risk has recently been questioned. Increasing atten-
tion has been focused on the role of the underlying
chronic inflammatory process as a major factor of
bone disease. In any case, the use of vitamin D and
calcium supplementation is highly recommended,
especially in those that have been steroid treated and
elderly patients. Bisphosphonate can be useful in
preventing and treating bone changes, but indica-
tions and selection of patients still remains unclear.
Further studies on genetic determinants of bone
changes in IBD could probably improve our ability in
selecting patients for appropriate treatment. On the
other hand, it has been shown that maintenance
therapy with infliximab can improve BMD, which
Nutrition and Malnutrition in Inflammatory Bowel Disease 115
underscores the role of inflammation in IBD-related
bone disease.
A nutritional approach in IBD, namely in Crohn’s
disease, is not just calorie supplementation [119]. It
is mainly recommended in children with active
Crohn’s disease, where it constitutes a major thera-
peutic tool, not only in improving nutritional status,
but also in favouring clinical remission, in sparing
or avoiding steroids, in allowing and accelerating
growth, in hastening the onset of puberty (especially
if the treatment is started early and in the prepuber-
tal period) and in improving school performance
and social activities. In Crohn’s disease, EN should
be preferred to parenteral treatment due to its lower
cost and side effects. Moreover, EN may have the
role of primary care in this disorder. Improvement
in intestinal permeability and modulation of the
inflammatory response are candidates for mecha-
nisms that have a positive effect in active Crohn’s
disease. An imbalance between Th1 and Th2 (and
related cytokines) is considered to be associated
with pathological response, and recognition of com-
mensal bacteria contributes to the Th1-Th2 cytokine
balance, underscoring that gut bacteria are neces-
sary for maintaining the immune homeostasis. This
balance is altered in Crohn’s disease, leading to
chronic inflammation. However, no information is
currently available on the effect of defined EN for-
mulas in modifying or modulating microflora and
related action on gut mucosa and inflammatory
response.
Comparable clinical results have been shared by
different EN formulas, and special formulas have not
shown any superiority over “regular” ones. Since the
basic composition of polymeric EN does not substan-
tially differ from foods and, although there is evi-
dence of actions on some inflammation-related
mechanisms, one might speculate whether the effect
is related to specific components, to some balance or
imbalance between them or whether it is aspecific
and related to the presence of nutrients in an
inflamed intestine.
In adult EN, although it offers some alternative to
drug therapy for inducing remission, in clinical prac-
tice it is actually restricted to patients suffering from
severe and persisting anorexia and from malnutri-
tion due to unremitting disease and/or complica-
tions. It has not proven to be effective in poor or non-
responders to first-line drug therapy, and few data
support its use in patients with suspected or effective
food intolerance, not amenable by means of food
exclusion diets.
Therapeutic improvement via infliximab in
inducing remission and in long-term management
of Crohn’s disease, in treating fistulas, and its role in
promoting better quality of life scores could restrict
indications for the nutritional approach as primary
care in Crohn’s disease. Nutritional care will proba-
bly maintain its role in children in complicated cases
in which drug therapy (namely steroids) can be
associated with a higher rate of long-term side
effects on growth, bone and endocrine system.
Mechanisms whereby EN formulas have a real ther-
apeutic effect on the immune and inflammatory
response represent an intriguing research field for
improving our understanding of the pathophysiolo-
gy of IBD. In a practical setting, oral nutrition
should always be preferred and promoted via nutri-
ent and energy dense foods with good calcium con-
tent, according to local nutritional habits and indi-
vidual preferences.
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Introduction
The rationale for using probiotics in inflammatory
bowel disease (IBD) is based on convincing evidence
implicating intestinal bacteria in their pathogenesis.
The distal ileum and the colon are the areas with the
highest bacterial concentrations and represent the
sites of inflammation in IBD; similarly pouchitis, the
non-specific inflammation of the ileal reservoir after
ileo-anal anastomosis, appears to be associated with
bacterial overgrowth and dysbiosis. Enteric bacteria
or their products have been found within the
inflamed mucosa of patients with Crohn's disease
(CD) [1].
There is evidence of a loss of immunologic toler-
ance to commensal bacteria in patients with IBD [2,
3]. Patients with CD respond consistently to diver-
sion of the faecal stream, with immediate recurrence
of inflammation after restoration of intestinal conti-
nuity [4] or infusion of luminal content into the
bypassed ileum [5], and pouchitis does not occur
before the ileostomy closure.
Patients with IBD have altered composition of
enteric flora with increase of aggressive bacteria such
as Bacterioides, adherent/invasive Escherichia coli,
Enterococci, and decrease of protective Lactobacillus
and Bifidobacterium species [6]. However, the most
compelling evidence is derived from animal models;
despite great diversity in genetic defects and
immunopathology, a consistent feature of many
transgenic and knockout mutant murine models of
colitis is dependency on the presence of normal
enteric flora for full expression of inflammation [7].
All these observations have suggested the possibility
of preventing or treating IBD by manipulating intes-
tinal microflora and increasing evidence supports the
potential therapeutic role of probiotics in IBD [8].
Probiotics
The first to propose the use of probiotics for the pur-
pose of health maintenance and disease prevention
was Elie Metchnikoff, the Russian Nobel Prize win-
ner, who at the turn of the last century suggested that
high concentration of Lactobacilli in the intestinal
flora was important for health and longevity in
humans [9]. Probiotics are defined as "living organ-
isms, which upon ingestion in certain numbers, exert
health benefits beyond inherent basic nutrition" [10].
Bacteria associated with probiotic activity are
most commonly Lactobacilli, Bifidobacteria and
Streptococci but other non-pathogenic bacteria such
as some strains of Escherichia coli and non-bacterial
organisms such as the yeast Saccharomyces boulardii
have been used (Table 1). For clinical application
probiotic strains must possess certain characteristics.
They need to be resistant to acid and bile, and must
have the ability to be metabolically active within the
luminal flora, where, ideally, they should survive, but
not persist in the long term. They should be antago-
nistic against pathogenic bacteria and, obviously,
they must be safe for human use and should main-
tain their viability and beneficial properties during
manufacturing processes [11].
Mechanisms of Action
Several mechanisms have been proposed to account
for probiotic action including the antagonistic activ-
ity against pathogenic bacteria either by inhibition of
adherence and translocation or by production of
anti-bacterial substances such as anti-microbial pep-
Probiotics in Inflammatory Bowel Diseases
Paolo Gionchetti, Fernando Rizzello, Claudia Morselli, Rosy Tambasco, Massimo Campieri
Table 1. Organisms associated with probiotic activity
Lactobacilli
Bifidobacteria
Streptococci
Others bacterial strains
Enterococci, non-pathogenic E. coli
Non bacterial organisms
Yeasts (Saccharomyces boulardii)
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