REVIEW

CURRENT
OPINION Inflammatory bowel disease and irritable bowel
syndrome: similarities and differences
Giovanni Barbara, Cesare Cremon, and Vincenzo Stanghellini

Purpose of review
Inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) are classically viewed as dichotomous
conditions. The former is perceived as a typical organic disease, and the latter is regarded as a disorder of
gut function driven by mood. Recent research identified some shared contributing factors, which will be
discussed here.
Recent findings
Mounting evidence shows the importance in both IBD and IBS of genetic, microbiological, epithelial, and
immunological factors. In some instances, these factors overlap in the two conditions as shown by:
involvement of brain–gut axis dysfunction in IBD, implication of TNFSF gene in Crohn’s disease and IBS,
evidence of abnormal microbiota and its impact on host functions, identification of low-grade inflammation
in subsets of IBS patients, and development of IBS symptoms in patients with IBD in remission.
Summary
IBD and IBS remain separate conditions although there are some overlapping mechanisms. Both research
and clinical management would benefit from considering a functional approach for certain manifestations
of IBD and accepting an organic view in subsets of IBS patients.
Keywords
epithelial barrier, genes, inflammatory bowel disease, irritable bowel syndrome, microbiota

INTRODUCTION substantiates points of contact and fuels the mount-

Inflammatory bowel disease (IBD) and irritable
bowel syndrome (IBS) are frequent gastrointestinal
conditions associated with a marked socioeconomic
burden and impairment of patients’ quality of life
& &
(QoL) [1 ,2 ]. IBD and IBS are clear paradigms of the
dichotomy between organic and nonorganic gastro-
intestinal diseases. IBD is classically viewed as a
peripheral condition characterized by intestinal
inflammation, responding to therapies that primar-
ily target the immune system. Conversely, IBS has
been considered for a long time a centrally driven
disorder diagnosed after exclusion of organic causes
and manageable with lifestyle modifications and
symptomatic treatment. However, several recent
findings indicate that the boundaries between IBD
and IBS are becoming blurred. There is epidemio-
logic, genetic, immune, and microbiological over-
lap. QoL is often similarly impaired in the two
conditions, and it is not uncommon to verify that
symptoms in patients with IBD surpass the severity
of endoscopic lesions and objective markers of
inflammation. The frequent experience of IBS-like
symptoms in patients with IBD in remission further
ing evidence supporting a role for immunological
dysfunction in the pathophysiology of IBS.
EPIDEMIOLOGICAL AND CLINICAL
FEATURES
IBD encompasses two main clinical entities, namely
ulcerative colitis and Crohn’s disease, both present-
ing commonly with abdominal pain, diarrhea, and
bloody stools. IBS is characterized by abdominal
pain/discomfort and disordered defecation and fur-
ther subtyped according to bowel habit character-
istics. The main subtypes are IBS with constipation
(IBS-C), IBS with diarrhea (IBS-D), and IBS with
Department of Medical and Surgical Sciences, University of Bologna,
Bologna, Italy
Correspondence to Giovanni Barbara, MD, Department of Medical and
Surgical Sciences, Section of Internal Medicine and Gastroenterology,
University of Bologna, St. Orsola–Malpighi Hospital, Building No. 5, Via
Massarenti, 9, I-40138, Italy. E-mail: giovanni.barbara@unibo.it
Curr Opin Gastroenterol 2014, 30:352–358
DOI:10.1097/MOG.0000000000000070

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Number 4
July 2014

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 Inflammatory bowel disease and irritable bowel syndrome Barbara et al.
KEY POINTS

IBD and IBS share some common features, including
the involvement of genetic factors, disorders of immune
system, and altered microbiota.

Some genetic polymorphisms (TNFSF15), which
regulate host–microbiota interactions, are more
frequently observed both in Crohn’s disease and IBS.

While low-grade intestinal inflammation has been
widely described in IBS, the magnitude and nature of
these responses is substantially different compared to
that of IBD.

IBS-like symptoms, which are frequently reported by
patients with IBD, originate from a combination of
psychological factors, low-grade inflammation, and
enteric neuroplastic changes.
mixed bowel habit features (IBS-M), although this
classification may be artificial as there is wide over-
&&
lap between these different entities [3 ]. Abdominal
pain, the cardinal symptom of IBS, is the first
reported complaint that induces patients to consult
a doctor and the key symptom impacting on QoL.
Pain is also very frequently reported by IBD patients
with active disease [4], but it is often neglected when
the therapeutic focus is on mucosal healing. How-
ever, pain becomes central in patients who continue
to complain of abdominal IBS-like symptoms in
spite of resolution of inflammation [4]. Both IBD
and IBS are associated with a significant impact on
physical as well as mental components of health-
& & &&
related QoL [1 ,2 ,5 ,6].
The prevalence of IBD has been estimated to
range between 1.5 and 294 cases per 100 000 people
[7]. Frequency figures are much higher for IBS
with around 10–20% of the population affected
in Europe and the United States [8]. There have been
similar trends of increasing prevalence of both IBD
&&
[5 ,9] and IBS [10] in the eastern world. It remains
unknown whether this is a primary epidemiological
shift of the disease or rather reflects higher consult-
ing rates, improvements in diagnosis, or the result of
increasing availability of therapeutic opportunities.
Although most patients with IBD seek medical
attention for their symptoms, there is an opposite
trend for IBS with the majority of patients non-
consulting a physician. While IBD impacts on both
outpatient and inpatient care, IBS is mainly seen in
&&
the outpatient setting [5 ]. Chronic constipation
and IBS together account for 9.4 million of the
11.6 million outpatient diagnoses for functional
gastrointestinal disorders (FGIDs) in the United
States [11]. In the female population, the rate visit
for IBS is 4.4 times that of males, making IBS the
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digestive disease with the greatest preponderance
among females [11]. Mortality is almost nonexistent
for IBS, but is also relatively rare for IBD, making
gastroesophageal reflux disease a more commonly
listed cause of death than IBD [11].
THE BRAIN–GUT AXIS
The brain–gut axis involves interactions among
the central and the autonomic nervous system,
the hypothalamic–pituitary–adrenal axis, and the
gastrointestinal tract, including the luminal
microbiota, the epithelial barrier, and the intestinal
immune system. Brain–gut axis interactions have
been typically studied in the context of FGIDs
and IBS in particular; however, several recent data
suggest their relevance also in the pathophysiology
&&
of IBD [12 ]. An association between psychological
factors and IBD flare-ups has been widely reported
&&
[12 ]. Depression has been shown to predispose to
higher inflammatory responses to a stressor [13 ],
&
and one third of patients report improvement of IBD
with antidepressant therapy [14]. Compared to con-
trols, patients taking antidepressants had reduced
relapse rates, steroid use, and endoscopic procedures
in the year after their introduction [15]. However,
confirmation of these data in prospective, con-
trolled studies is lacking. FGIDs have been widely
linked to psychological factors, including anxiety,
depression, fobia, and somatization. Koloski et al.
&
[16 ] performed a 12-year longitudinal, prospective,
population-based study to determine the direction-
ality of brain–gut interactions in IBS and functional
dyspepsia. As expected, higher levels of anxiety and
depression at baseline were predictive of IBS at
follow-up. However, FGID without mood disorders
at baseline predisposed individuals to anxiety and
depression at follow-up, suggesting that peripheral
changes may be the trigger of mood disorders at least
in a subgroup of IBS patients. Interestingly, disease
activity status and severity of inflammation have
also been linked to the severity of psychological
symptoms associated with IBD (e.g. anxiety and
&&
depression) [12 ]. Regional cortical gray matter
density changes have been detected in diverse
inflammatory disorders, including IBD and IBS.
The importance of female sex in brain neuroplastic
changes has been described, particularly in IBS
[17,18]. Recent data suggest that these changes
could be the consequence of peripheral gut inflam-
mation in ulcerative colitis, whereas they may
represent a primary pathogenetic factor in IBS
[17]. However, convincing cause–effect relationship
in these disorders is still lacking. One major con-
tributor of brain responses and symptom perception
in IBS is visceral hypersensitivity, the increased
www.co-gastroenterology.com 353
 Inflammatory bowel disease
perception of stimuli arising from the gastrointesti-
nal tract [19]. The role of visceral hypersensitivity
and its correlation with the degree of active inflam-
mation is controversial [20]. On the other hand,
visceral hypersensitivity may become more evident
in patients with IBD in clinical remission who show
persistent symptoms including abdominal pain
&&
[21 ].
GENETIC FACTORS
Gene hunting started over a decade ago in IBD
research and led to identification of several genes
contributing to IBD pathogenesis. These findings
substantiate the known familiar aggregation in
these patients. A recent meta-analysis of genome-
wide association studies identified 163 susceptibility
loci in IBD. Many of these loci (e.g. NOD2, IRGM,
ATG16L1, and IL23R) are involved in host–micro-
biota interactions [22]. The TNFSF15 gene encodes
for TL1A, a member of the TNF ligand superfamily
that is involved in defense against pathogens and
modulates the interactions between host and micro-
biota in the gut. The TNFSF15 gene was first ident-
ified as a risk factor for Crohn’s disease and later
reported to also contribute to the risk of ulcerative
colitis [22]. On the basis of the observation that a
subgroup of patients with IBS shows evidence of
low-grade immune activation, the involvement of
TNFSF15, previously linked to Crohn’s disease, has
been recently investigated. A large IBS case–control
study in 1992 individuals from two independent
cohorts from Sweden and the United States ident-
ified that the Crohn’s disease-risk variant G from the
rs4263839 single nucleotide polymorphism (SNP) in
the TNFSF15 gene was more frequently observed
in IBS (particularly IBS-C) than controls [23]. These
data have been recently confirmed in a smaller study
from the United Kingdom demonstrating also a
higher tissue expression of TNFSF15 along with
increased mRNA expression of several cytokines
and chemokines [24]. As the disease risk alleles
may be the same for Crohn’s disease and IBS, it
has been hypothesized that common mechanisms
could be involved in the predisposition to both
conditions. It has also been hypothesized that IBS
may represent an immunologically incomplete
expression variant of Crohn’s disease [18]. Along
the line of an involvement of genes in the patho-
genesis of IBS, it was found that development of IBS
following a waterborne outbreak of infectious gas-
troenteritis was associated with SNPs in toll-like
receptor 9 (TLR9), the tight junction protein cad-
herin (CDH1), and the pro-inflammatory cytokine
interleukin 6, which are involved in host–micro-
biota interactions, epithelial barrier, and immune
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activation [25]. Although these data suggest that IBS,
similarly to IBD, is linked to an abnormal mucosal
immune response to luminal microbiota in geneti-
cally predisposed individuals, more work has to be
done to confirm or discard this interesting hypo-
thesis. Nonetheless, these data support the concept
of a central role for organic changes in the patho-
genesis of at least a subgroup of patients with IBS.
MICROBIOTA
It is well established that IBD patients show reduced
diversity and different compositions of intestinal
microbiota, including reduction of bacteria
involved in butyrate and propionate metabolism
(e.g. Ruminococcus bromii et rel., Eubacterium rectale
et rel., and Roseburia sp.) as well as mucus degra-
& &
dation (i.e. Akkermansia sp.) [26 –28 ]. Attention
has been also directed to the potential role of
specific bacterial strains including the reduction
in tissue concentrations of the anti-inflammatory
microbiota commensal Faecalibacterium prausnitzii
&
[26 ]. The pathogenetic role of F. prausnitzii in IBD
is supported by data showing that low tissue con-
centration of this bacterium was associated with an
increased risk of postoperative recurrence of Crohn’s
&
disease [26 ]. However, a recent study failed to find
decreased tissue levels of F. prausnitzii at least in a
pediatric group of Crohn’s disease patients [29]. The
evidence linking microbiota to IBS is in its infancy,
&&
but it is already providing exciting results [30 ]. The
clearest evidence of the participation of bacteria in
the pathogenesis of IBS is provided by the fact that
about 10% of individuals experiencing an acute
episode of gastroenteritis (e.g. Shigella, Salmonella,
and Campylobacter) develop persistent symptoms
fulfilling the criteria for IBS [31]. A 16-year, prospec-
tive, controlled, culture-proven, follow-up study
explored the association between a single episode
of Salmonella gastroenteritis and new-onset FGIDs.
In this long-term outcome study, it was shown that
Salmonella gastroenteritis increased the risk for IBS,
but only if the infection occurred during childhood
&
[32 ]. Interestingly, acute infectious gastroenteritis
is also a trigger for the development of IBD [33].
Porter et al. [33] demonstrated that acute infectious
gastroenteritis was an independently associated risk
factor for IBD [odds ratio (OR): 1.40] with ORs for
Crohn’s disease slightly higher than those for ulcer-
ative colitis (ORs: 1.54 and 1.36, respectively).
The first compelling evidence of altered fecal
microbiota composition in IBS comes from a Finnish
study showing increased ratio of Firmicutes:Bacter-
oidetes and lower levels of Bifidobacteria [34]. A
recent study investigated the correlation between
microbiota profiles and psychological factors or
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 Inflammatory bowel disease and irritable bowel syndrome Barbara et al.
&&
bowel physiology [35 ]. It was found that micro-
biota abnormalities were associated with peripheral
changes such as disturbances in gut transit, whereas
individuals with no modifications of the microbiota
&&
correlated with anxiety and depression [35 ]. More
recently, a bacterial profile of 27 genus-like groups
significantly separated both postinfectious IBS and
IBS-D from controls. The study also provided evi-
dence of a correlation between changes in micro-
biota and expression of several host gene pathways
involved in impaired epithelial barrier function
&&
[36 ]. Attention is being directed to the potential
functional consequences of altered microbiota taxa.
Diet is a major driving force in the control of micro-
biota composition and function. On the other hand,
microbiota changes may lead to the abnormal
fermentation of indigestible carbohydrates, with
consequent production of gas and metabolites
potentially involved in symptom generation. The
effect of a challenge with a diet rich in fibers on
microbiota composition and abdominal symptoms
has been recently investigated. When patients com-
plaining of flatulence were challenged with the
fiber-rich diet, microbiota showed higher instability
and reduction of microbial diversity compared to
healthy controls. In addition, when challenged,
both groups recorded more abdominal symptoms,
number of gas evacuations, and more gas pro-
&
duction [37 ]. Previous data demonstrated increased
luminal and fecal protease activity in IBS. Proteases
have been linked to the activation of receptors that
are involved in pain transmission and bowel dys-
function. Specific intestinal bacterial groups (Lacto-
bacillales, Lachnospiraceae, and Streptococcaceae) are
linked to fecal protease activity. These data support
the hypothesis that bacteria could be important
contributors to higher fecal protease activity and
support a link between bacteria and abdominal pain
[38].
EPITHELIAL BARRIER
The intestinal barrier represents a strategic site of the
interplay between billions of bacteria, nutrients, and
the host. A long-term change in epithelial barrier
function has been suggested to play a role in the
pathogenesis of IBD and predispose to IBD relapses
[39]. Increased intestinal permeability has been
recently suggested to participate in the pathogenesis
of symptoms in IBS [40]. Higher paracellular per-
meability was demonstrated in colonic biopsies
in Ussing chamber experiments [41]. In Caco-2
monolayers, the application of cleared supernatants
of IBS colonic biopsies in culture induced down-
regulation of zonula occludens-1 mRNA expression
and increased paracellular permeability, which
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correlated with the severity of abdominal pain
[41,42]. These functional observations are accom-
panied by elegant morphological studies showing
that the jejunal mucosa of patients with IBS-D
showed alterations in expression and phosphoryl-
ation of tight junctions and ultrastructural abnor-
malities such as perijunctional cytoskeleton con-
densation and enlarged apical intercellular distance
&
between cells [43 ]. Interestingly, these alterations
were correlated both with mast cell activation and
clinical symptoms including diarrhea and pain
&
severity [43 ]. The cause(s) of the described morpho-
logical and functional changes remain unknown,
although previous episodes of infectious gastroen-
teritis, dysbiosis, allergy, genetic, and epigenetic
factors may be involved. Low-grade inflammation
described in subgroups of patients with IBS may
have a role in the maintenance of increase of
intestinal permeability.
INFLAMMATION
Tissue inflammation is central to IBD pathogenesis
and has been the starting point of mainstream
research in this condition. Conversely, the concept
that IBS pathogenesis involves peripheral organic
changes and minimal inflammation is relatively
new and represents a new concept resulting from
recent research. Several studies showed increased
numbers of immunocytes (e.g. mast cells and T cells)
in both adult and pediatric IBS [44]. Low-grade
inflammation has been mainly associated with post-
infectious IBS; however, several studies demonstrate
similar findings in IBS-D and IBS-C [45]. The fact
that up to one third of patients with IBD in remis-
sion and around half of patients with microscopic
colitis experience IBS-like symptoms further sup-
ports the involvement of low-grade inflammation
in IBS [44]. Low-grade inflammation is coupled
with increased expression of innate immunity to
microbial molecular patterns (e.g. TLR) [46],
suggesting a contributing role for gut microbiota.
Biopsies obtained from the colonic mucosa of IBS
patients released higher amounts of inflammatory
mediators, including proteases, histamine, and
prostaglandins compared with controls [47–49].
Caution should be used when comparing this
inflammatory response with that of IBD, as marked
quantitative and qualitative differences exist. As
expected, the magnitude of the inflammatory
response seen in IBS was much lower than that of
active or quiescent ulcerative colitis, although it was
widely overlapping with that of microscopic colitis
[50]. In IBS, most data converge on the implication
of mast cells. Activated mast cells in close proximity
of enteric nerves were correlated with the intensity
www.co-gastroenterology.com 355
 Inflammatory bowel disease
and frequency of abdominal pain [49]. Mucosal
mediators of mast cell origin hyperexcited nocicep-
tive visceral sensory pathways in recipient rodents
&
[47,48,51 ] or enteric nervous system excitability in
isolated gut tissues from guinea pigs [52]. Although
immune cells are likely the major source of mediators
impacting nerve function, a microbial origin of some
of these factors has also been suggested [53]. Potential
contributing factors of this low-grade inflammation
include, among others, allergic reactions and stress.
Acute psychological stress increased small intestinal
permeability in humans and the mast cell stabilizer
disodium chromoglycate blocked this effect. These
findings provide new insights into the complex inter-
play between the central nervous system and the
immune system in humans [54].
EXPERIENCE OF IRRITABLE BOWEL
SYNDROME SYMPTOMS IN PATIENTS
WITH INFLAMMATORY BOWEL DISEASE
IN REMISSION
Although a high proportion of patients with IBD
frequently experiences symptoms, which are indis-
tinguishable from IBS, the diagnosis is generally
confirmed by additional laboratory and imaging
studies. The clinical dilemma emerges when
patients continue to experience symptoms (e.g.
abdominal pain, bloating and changes in bowel
habit) while in remission. Is this the expression of
occult active disease or IBS? Should these patients
receive more aggressive anti-inflammatory/immuno-
suppressive therapy?
A meta-analysis of 1703 individuals showed that
the prevalence of IBS-like symptoms in patients with
IBD in remission was 35%. Crohn’s disease patients
in remission had a higher risk of having IBS-like
symptoms compared with ulcerative colitis in remis-
sion (OR: 1.74; 95% CI: 1.24 – 2.43) [4]. IBS-like
symptoms in these individuals were associated with
female sex, reduced well-being, and QoL as well as
higher fatigue scores than those without [21 ].
&&
Nonetheless, a comparative study reported that
QoL was more severely affected in ‘true’ IBS com-
pared with IBS occurring in IBD patients in remis-
sion. In a recent longitudinal 3-year follow-up
study, it was observed that symptoms of IBS in
ulcerative colitis in remission tended to fluctuate
over time being present overall in 19% of patients at
&&
yearly visits [21 ]. A frequent finding is the detec-
tion of higher levels of mood disorders, including
predominantly anxiety, in patients experiencing
IBS-like symptoms compared with symptom-free
&&
individuals [4,21 ]. Although anxiety was inde-
pendently associated with IBS symptoms, the
risk seems moderate (OR: 1.11, CI: 1.01–1.21),
356 www.co-gastroenterology.com
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suggesting that central factors alone cannot justify
completely the development of IBS-like symptoms
in all patients [4].
The prevalence of IBS in the general population is
relatively high (10–20%), hence coexistent IBS could
be expected in a similar proportion of IBD patients in
remission. However, the high prevalence of IBS-like
symptoms in IBD in remission cannot be explained
by casual overlap alone. Whether IBS-like symptoms
reflect clinically undetected, low-grade inflam-
mation is a matter of controversy. Fecal calprotectin
was significantly higher in Crohn’s disease and ulcer-
ative colitis patients with criteria for IBS than in
those without IBS-type symptoms [55]. In addition,
increased intraepithelial lymphocytes and tissue
tumor necrosis factor alpha expression was associated
with IBS-like symptoms in quiescent IBD, but not
&&
with IBS [56 ]. These findings suggest that occult
inflammation could drive IBS-like symptoms in
patients with IBD in remission and imply the possible
need of further testing (e.g. fecal calprotectin) and
potentiation of immunosuppressive therapy [55].
However, increased calprotectin levels have not been
confirmed in more recent studies, suggesting a more
&&
complex pathogenesis [4,21 ]. A barostat study in
patients with ulcerative colitis in remission indicated
that IBS-like symptoms were associated with visceral
hypersensitivity and mast cell infiltration [57]. In
addition, Akbar et al. [58] showed a 3.9-fold to 5-fold
increase of the sensory nerve receptor transient
receptor potential vanilloid type 1 (TRPV1) associ-
ated with pain perception in the mucosa of IBD
patients with IBS symptoms. TRPV1 expression cor-
related with the severity of abdominal pain, suggest-
ing that postinflammatory neuroplastic changes
occurring at least in a subgroup of patients with
IBD may have potential consequences for bowel
physiology, visceral hypersensitivity, and symptom
generation.
CONCLUSION
Recent research suggests that IBD and IBS share
some common pathogenetic features. The possible
implication of microbiota, inflammation, and
genetic factors has received increasing attention
in IBS research, although their relevance is far less
defined in IBS compared with IBD. The overlap
between IBD and IBS is particularly evident in
patients who develop IBS-like symptoms while in
remission. A better understanding of the role of
pathogenetic factors and mechanisms underlying
the development of persistent symptoms in patients
with IBD in remission is now needed for the identi-
fication of more objective disease signatures and
development of targeted therapies.
Volume 30
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 Inflammatory bowel disease and irritable bowel syndrome Barbara et al.
Acknowledgements
G.B. and V.S. are supported in part by the Italian
Ministry of Instruction, University and Research.
Conflicts of interest
G.B. and V.S. have served as consultants/advisory board
members for Alfa Wassermann, Almirall, Italchimici,
Ironwood, and Shire. G.B. and V.S. received research
grant support from Alfa Wassermann, Italchimici, and
Shire. G.B. received research grant support from Falk
Pharma, Sofar, and Yakult. V.S. received research grant
support from Almirall, Aptalis, Norgine, and Valeas.
G.B. served as consultant/advisory board member for
Danone, Falk Pharma, Malesci, Nestlè, Noos, Sofar,
Synergy, and Yakult. V.S. served as consultant/advisory
board member for Angelini, Aptalis, CM&D Pharma,
Farmaderma, Janssen, Norgine, Takeda, Valeas, and
Zeria. C.C. has been the recipient of a scholarship grant
from Sofar.
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Important report characterizing IBS-like symptoms in patients with ulcerative colitis
in clinical remission and their correlation with inflammatory markers, psychological
symptoms, and QoL. IBS-like symptoms are common in these patients and are
associated with poor psychological well-being and reduced QoL.
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bowel syndrome and the role of microbiota modulation in these disorders.
27. Cader MZ, Kaser A. Recent advances in inflammatory bowel disease:
& mucosal immune cells in intestinal inflammation. Gut 2013; 62:1653–
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Up-to-date review highlighting the complex interplay of distinct intestinal immune
cell types and discussing how mucosal immune system perturbations can lead to
inflammation.
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& of dysbiosis in ulcerative colitis during remission. Inflamm Bowel Dis 2013;
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Interesting study assessing fecal microbiota composition in patients with ulcerative
colitis. Results showed that fecal microbiota composition differs significantly in
these patients in comparison with controls, but it is stable in time. This dysbiosis is
characterized by significant reduction of members of the Clostridium cluster IV and
significant reduction of bacteria involved in butyrate and propionate metabolism,
including Ruminococcus bromii et rel., Eubacterium rectale et rel., Roseburia sp.,
and Akkermansia.
29. Hansen R, Russell RK, Reiff C, et al. Microbiota of de-novo pediatric IBD:
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In depth review on the current knowledge on the role of intestinal microbiota in the
pathophysiology of functional gastrointestinal disorders. The review explores also
treatment implications including the use of prebiotics, probiotics, symbiotics, and
antibiotics in these syndromes.
31. Spiller R, Garsed K. Postinfectious irritable bowel syndrome. Gastroenterol-
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Prospective, controlled, cohort study assessing functional digestive symptoms,
psychological factors, and QoL 16 years after a single culture-proven foodborne
Salmonella enteritidis outbreak involving 1811, mostly pediatric, patients in
Bologna, Italy. Acute Salmonella gastroenteritis was identified as a risk factor
for the development of long-term IBS symptoms (OR for IBS 1.92; 95% CI: 1.23–
2.98), but only if the infection occurs during childhood (OR for IBS in children 2.12;
95% CI: 1.21–3.71).
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35. Jeffery IB, O’Toole PW, Öhman L, et al. An irritable bowel syndrome subtype
&& defined by species-specific alterations in faecal microbiota. Gut 2012;
61:997–1006.
Interesting study investigating the association between microbiota and the brain–
gut axis in patients with IBS. Results showed that those with no modifications in
fecal microbiota had more mood disorders while those with modification in
microbiota had changes in bowel physiology.
36. Jalanka-Tuovinen J, Salojarvi J, Salonen A, et al. Faecal microbiota composi-
&& tion and host–-microbe cross-talk following gastroenteritis and in postinfec-
tious irritable bowel syndrome. Gut 2013. [Epub ahead of print]
First study to show that fecal microbiota of patients with postinfectious
IBS differs from that of controls and shares similarities with that of patients
with IBS with diarrhea, suggesting a common pathophysiology. Members of
Bacteroidetes phylum were increased 12-fold in patients, while controls had
35-fold more uncultured Clostridia. Microbial dysbiosis correlates with the
expression of several host gene pathways, including impaired epithelial barrier
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Study analyzing the potential role of diet on digestive symptoms, anal gas
evacuation, intestinal gas distribution, and colonic microbiota in 30 patients with
flatulence. On a flatulogenic diet, both patients and controls recorded more
abdominal symptoms, gas production, and evacuations. Interestingly, only micro-
biota of patients developed instability in composition, while that of controls was
stable, suggesting that patients with flatulence have a poor tolerance of intestinal
gas that is associated with microbiota instability.
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& syndrome: an organic disorder with structural abnormalities in the jejunal
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Careful study assessing clinical symptoms and jejunal biopsies in 45 patients with
IBS-D and 30 controls. Patients with IBS-D displayed increased mast cell counts and
activation, increased protein expression of claudin-2, reduced occludin phosphor-
ylation and enhanced redistribution from the membrane to the cytoplasm, increased
myosin kinase expression, and enhanced phosphorylation of myosin. These altera-
tions were associated with ultrastructural abnormalities at the apical junction complex
which correlated both with mast cell activation and clinical symptoms.
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terology 2007; 132:26–37.
49. Barbara G, Stanghellini V, De Giorgio R, et al. Activated mast cells in proximity
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& peripheral sensory nerves by mediators from colonic biopsies of diarrhea-
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Study examining the impact of mediators from colonic biopsies of patients with IBS
on intrinsic excitability of colonic nociceptive dorsal root ganglion neurons. Super-
natants from patients with IBS-D but not IBS-C induced a marked increase in
neuronal excitability by a protease-activated receptor 2-mediated mechanism.
52. Balestra B, Vicini R, Cremon C, et al. Colonic mucosal mediators from patients
with irritable bowel syndrome excite enteric cholinergic motor neurons.
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53. Steck N, Mueller K, Schemann M, Haller D. Bacterial proteases in IBD and
IBS. Gut 2012; 61:1610–1618.
54. Vanuytsel T, van Wanrooy S, Vanheel H, et al. Psychological stress and
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56. Vivinus-Nebot M, Frin-Mathy G, Bzioueche H, et al. Functional bowel symp-
&& toms in quiescent inflammatory bowel diseases: role of epithelial barrier
disruption and low-grade inflammation. Gut 2014; 63:744–752.
Important study evaluating the role of colonic barrier defects and low-grade
inflammation in cecal biopsies of 51 patients with IBS, 49 patients with quiescent
IBD and 27 controls. Paracellular permeability was significantly increased in IBS
and patients with quiescent IBD and IBS-like symptoms and associated with lower
expression of ZO-1 and a-catenin. Intraepithelial lymphocytes and TNFa were
significantly increased only in patients with quiescent IBD and IBS-like symptoms.
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58. Akbar A, Yiangou Y, Facer P, et al. Expression of the TRPV1 receptor differs in
quiescent inflammatory bowel disease with or without abdominal pain. Gut
2010; 59:767–774.
Volume 30
Number 4
July 2014