MUCOSAL CYTOKINE PRODUCTION IN SMALL-INTESTINAL BACTERIAL OVERGROWTH

Citation
Sm. Riordan et al., MUCOSAL CYTOKINE PRODUCTION IN SMALL-INTESTINAL BACTERIAL OVERGROWTH, Scandinavian journal of gastroenterology, 31(10), 1996, pp. 977-984
Citations number
39
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
00365521
Volume
31
Issue
10
Year of publication
1996
Pages
977 - 984
Database
ISI
SICI code
0036-5521(1996)31:10<977:MCPISB>2.0.ZU;2-W
Abstract
Background: Mucosal production of interferon-gamma, interleukin-6, and tumour necrosis factor-alpha is increased in inflammatory bowel disea se and parallels disease activity. Interferon-gamma production is also increased in coeliac disease. Conversely, local cytokine profiles hav e not been investigated in small-intestinal bacterial overgrowth. This study addressed this issue. Methods: Eighteen adult subjects were stu died with culture of proximal small-intestinal luminal secretions and measurement of luminal interferon-gamma, interleukin-6, and tumour nec rosis factor-alpha concentrations by enzyme-linked immunosorbent assay . Small-intestinal histology was assessed by light microscopy. Results : Interferon-gamma, interleukin-6, and tumour necrosis factor-alpha we re measurable in proximal small-intestinal luminal secretions of all s ubjects, even in the absence of light microscopic evidence of enteropa thy. Small-intestinal bacterial overgrowth was present in 12 of 18 (66 .7%) subjects. Luminal concentrations of neither interferon-gamma nor tumour necrosis factor-alpha differed significantly in subjects with a nd without small-intestinal bacterial overgrowth (P = 0.06 and P = 1.0 , respectively). Conversely, luminal interleukin-6 concentrations were significantly increased in subjects with this disorder (P = 0.02). Mu ltivariate linear regression analysis suggested that colonic-type rath er than salivary-type flora mediated this increased interleukin-6 resp onse (P = 0.02 and P = 0.64, respectively). No correlation was found b etween luminal interleukin-6 and tumour necrosis factor-alpha concentr ations, even after the confounding influence of colonic-type bacteria was excluded (P = 0.60). Conclusions: These findings suggest that incr eased mucosal production of interleukin-6 occurs in small-intestinal b acterial overgrowth, particularly when the overgrowth flora includes c olonic-type bacteria. Conversely, luminal levels of neither interferon -gamma nor tumour necrosis factor-alpha are increased in this circumst ance, distinguishing the local cytokine profile in this disorder from those that occur in coeliac disease and inflammatory bowel disease.