2002
DOI: 10.1053/gast.2002.34097
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A case for an immunological basis for irritable bowel syndrome

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Cited by 70 publications
(43 citation statements)
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“…Animal studies suggest that stress may enhance responsiveness to inflammatory stimuli in the gut, while inflammatory processes in the gut may influence behavior and brain function. [41][42][43][44] The close proximity of chronic inflammatory cells to enteric nerves in the mucosa 36,37 and muscularis externa 27 of patients with IBS, provides an interface for direct interaction between cells and the enteric nervous system. Potential mechanisms of immune activation in IBS that have been suggested include a previous episode of gastroenteritis, alterations in intestinal microflora, undiagnosed food allergies and genetic factors.…”
Section: Morphologic Changes and Pathophysiology Of Ibsmentioning
confidence: 99%
“…Animal studies suggest that stress may enhance responsiveness to inflammatory stimuli in the gut, while inflammatory processes in the gut may influence behavior and brain function. [41][42][43][44] The close proximity of chronic inflammatory cells to enteric nerves in the mucosa 36,37 and muscularis externa 27 of patients with IBS, provides an interface for direct interaction between cells and the enteric nervous system. Potential mechanisms of immune activation in IBS that have been suggested include a previous episode of gastroenteritis, alterations in intestinal microflora, undiagnosed food allergies and genetic factors.…”
Section: Morphologic Changes and Pathophysiology Of Ibsmentioning
confidence: 99%
“…Surprisingly, given the aforementioned description of a direct relationship between symptoms and chronic inflammation among patients with post-infectious IBS, these authors did not find an association between either the nature of disease onset or disease duration and immunological findings. In an accompanying editorial, Collins suggested that the increased presence of CD25+ cells may have indicated "auto-or exogenous antigen challenge in these patients, and that the CD25+ cells are preventing the progression to a more florid inflammatory response" [33] . That IBS patients may be predisposed to an, albeit contained, inflammatory response to luminal triggers is also supported by the finding, of Gonsalkorale and colleagues, of a reduced frequency of the high-producer phenotype for the antiinflammatory cytokine interleukin-10 (IL-10) among IBS patients [9] .…”
Section: Infection Inflammation Immunity and Ibsmentioning
confidence: 99%
“…It is attractive to suggest that these immunological changes could result from exposure to an exogenous (such as bacterial) antigen challenge (50,51). That IBS patients may be predisposed to an, albeit contained, inflammatory response to luminal triggers is, indeed, supported by the finding of polymorphisms in genes that encode for the production of anti-inflammatory cytokines among IBS patients (52,53) and by the very recent description of high titers of anti-flagellin antibodies in serum derived from IBS patients (54,55).…”
Section: Inflammation and Ibsmentioning
confidence: 99%