Role of infection in irritable bowel syndrome

Spiller, Robin C.

doi:10.1007/s00535-006-1925-8

Cited by 187Gastrointestinal motility and disordersGut microbiota and healthMicroscopic Colitis

Role of infection in irritable bowel syndrome

Spiller, Robin C.·2007·Journal of Gastroenterology

DOI 10.1007/s00535-006-1925-8

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Abstract

Infection by pathogenic organisms leads to mucosal damage and disruption of the gut's extensive commensal flora, factors which may lead to prolonged bowel dysfunction. Six to 17% of unselected irritable bowel syndrome (IBS) patients believe their symptoms began with an infection, which is supported by prospective studies showing a 4%-31% incidence of postinfectious IBS-(PI) following bacterial gastroenteritis. The wide range of incidence can be accounted for by differences in risk factors, which include in order of magnitude; severity of initial illness > bacterial toxigenicity > hypochondriasis, depression and neuroticism, and adverse life events in the previous 3 months. PI-IBS has been reported after Campylobacter, Salmonella, and Shigella infections. Serial biopsies after Campylobacter jejuni gastroenteritis show an initial inflammatory infiltrate, with an increase in enterochromaffin (EC) cells, which in most cases subsides over the next 6 months. Those who go on to develop IBS show increased numbers of EC and lymphocyte cell counts at 3 months compared with those who do not develop IBS. Interleukin-1beta mRNA levels are increased in the mucosa of those who develop PI-IBS, who also show increased gut permeability. Recover can be slow, with approximately 50% still having symptoms at 5 years. Recent studies suggest an increase in peripheral blood mononuclear cell cytokine production in unselected IBS, an abnormality that may be ameliorated by probiotic treatment. The role of small-bowel bacterial overgrowth in IBS is controversial, but broad-spectrum antibiotics do have a temporary benefit in some patients. More acceptable long-term treatments altering gut flora are awaited with interest.

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As a consequence, serotonin receptors on enterocytes and on intrinsic and extrinsic primary nerve endings are activated in a paracrine fashion.
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Authors: Spiller, R. C.
Venue: Journal of Gastroenterology
Publisher: Springer Science and Business Media LLC
Published: 2007-01-19
Volume: 42
Issue: S17
Pages: 41-47
ISSN: 0944-1174 (ISSN-L)
1435-5922
DOI: 10.1007/s00535-006-1925-8
OpenAlex: W1984468996
Cited by: 187
References: 53
Citations by year: 2026: 1 · 2025: 3 · 2024: 3 · 2023: 2 · 2022: 3 · 2021: 3 · 2020: 5 · 2019: 8 · 2018: 6 · 2017: 8 · 2016: 8 · 2015: 13 · 2014: 18 · 2013: 12 · 2012: 15
FWCI: 3.84
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Journal of Gastroenterology (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
Health Sciences › Medicine › Epidemiology › Microscopic Colitis
Keywords: irritable bowel syndrome, bacterial gastroenteritis, Campylobacter jejuni, Salmonella, Shigella, enterochromaffin cells, intestinal permeability, IL-1β, cytokine production, probiotics, small intestinal bacterial overgrowth, broad-spectrum antibiotics, gut microbiota, bowel dysfunction, risk factors
MeSH terms: Bacterial Infections, Humans, Serotonin, Gastrointestinal Tract, Irritable Bowel Syndrome

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Role of infection in irritable bowel syndrome

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