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Cited by 144Salmonella and Campylobacter epidemiologyGastrointestinal motility and disordersHelicobacter pylori-related gastroenterology studies

Relationship of Campylobacter Toxigenicity In Vitro to the Development of Postinfectious Irritable Bowel Syndrome

Thornley, Jonathan P., Jenkins, David, Neal, Keith, Wright, Trina, Brough, Jo, Spiller, Robin C.·2001·The Journal of Infectious Diseases
DOI 10.1086/322845
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Abstract

Campylobacter enteritis is associated with a significant risk of developing irritable bowel syndrome, but the mechanism is unknown. This study ascertained bowel symptoms in 93 patients 3 months after Campylobacter jejuni enteritis infection. The infecting organisms were cultured, and the effects of culture supernatants on toxin-sensitive epithelial cell monolayers (HEp-2, Green monkey kidney epithelial [Vero], and CHO-K1) were investigated. In all, 50, 43, and 41 of the isolates showed toxigenic effects on HEp-2, CHO-K1, and Vero cells, respectively. Persistently changed bowel habit was reported by 9 of 50 persons with HEp-2 toxin-positive infections but by only 2 of 43 with isolates negative for toxin (chi2=4.0; P<.05). Toxicity to HEp-2 and Vero cells was associated with significantly increased numbers of days with loose stools 6 months after C. jejuni enteritis infection (both, P<.05). Thus, long-term symptoms that occur Campylobacter infection are significantly associated with bacterial toxicity.

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  • The strongest risk factors for post-infectious irritable bowel syndrome are bacterial toxicity, prolonged duration of diarrhoea, rectal bleeding and fever.

    “in which the strongest risk factors are bacterial toxicity,128 prolonged duration of diarrhoea,124 rectal bleeding129 and fever.125”

    From Intestinal microbiota in functional bowel disorders: a Rome foundation report (2013) · cites this paper as [128]

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Research works printed but not linked: 2

  1. Drossman DA, Thompson WG, Talley NJ, Funch-Jensen P, Janssens J, Whitehead WE. Identification of sub-groups of functional gastrointestinal disorders. Gastroenterol Int 1990; 3:159-72.
  2. Jenkins D, Thornley JP, Wright T, et al. Enterchromaffin and mast cell hyper- plasia parallels mucosal nerve damage following Campylobacter enteritis. Neurogastroenterol Motil 1998; 10:464.

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Authors
Thornley, J. P., Jenkins, D., Neal, K., Wright, T., Brough, J., & Spiller, R. C.
Affiliations
  • Nottingham University Hospitals NHS Trust (GB)
  • University of Nottingham (GB)
ORCID
Venue
The Journal of Infectious Diseases
Publisher
Oxford University Press (OUP)
Published
2001-09
Volume
184
Issue
5
Pages
606-609
ISSN
  • 0022-1899 (ISSN-L)
  • 1537-6613
DOI
10.1086/322845
OpenAlex
W2144481594
Cited by
144
References
15
Citations by year
2025: 1 · 2024: 2 · 2023: 2 · 2022: 4 · 2021: 2 · 2020: 2 · 2019: 3 · 2018: 6 · 2016: 4 · 2015: 1 · 2014: 12 · 2013: 6 · 2012: 10
FWCI
9.76
Type
journal article
Language
en
Open access
closed
Locations
  • The Journal of Infectious Diseases (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Agricultural and Biological Sciences › Food Science › Salmonella and Campylobacter epidemiology
  • Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
  • Health Sciences › Medicine › Surgery › Helicobacter pylori-related gastroenterology studies
Keywords
Campylobacter jejuni, post-infectious irritable bowel syndrome, bacterial toxins, enteritis, HEp-2 cells, Vero cells, CHO-K1 cells, loose stools
MeSH terms
Adolescent, Adult, Animals, Bacterial Toxins, Campylobacter Infections, Cell Line, Chlorocebus aethiops, Colonic Diseases, Functional, Enteritis, Epithelial Cells, Cricetinae, Humans, Vero Cells, Campylobacter jejuni, CHO Cells

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