Bifidobacterium animalis causes extensive duodenitis and mild colonic inflammation in monoassociated interleukin-10-deficient mice
Article first published online: 23 FEB 2009
Copyright © 2009 Crohn's & Colitis Foundation of America, Inc.
Inflammatory Bowel Diseases
Volume 15, Issue 7, pages 1022–1031, July 2009
How to Cite
Moran, J. P., Walter, J., Tannock, G. W., Tonkonogy, S. L. and Sartor, R. B. (2009), Bifidobacterium animalis causes extensive duodenitis and mild colonic inflammation in monoassociated interleukin-10-deficient mice. Inflamm Bowel Dis, 15: 1022–1031. doi: 10.1002/ibd.20900
- Issue published online: 10 JUN 2009
- Article first published online: 23 FEB 2009
- Manuscript Accepted: 19 JAN 2009
- Manuscript Received: 15 JAN 2009
- NIH. Grant Number: R01 DK53347
- National Institute of General Medical Sciences. Grant Number: GM 00678
- Center for Gastrointestinal Biology and Disease (CGIBD). Grant Number: P30 DK 034987
- National Gnotobiotic Rodent Resource Center. Grant Number: P40 R018603
- intestinal inflammation;
- animal models;
- IL-10 deficient mice;
- Bifidobacterium animalis
Background: We recently showed that Bifidobacterium animalis is more prevalent within the colons of interleukin (IL)-10-deficient (−/−) mice than in wildtype (WT) animals colonized with the same specific pathogen-free (SPF) fecal contents. Here we tested the ability of this organism to cause T-cell-mediated intestinal inflammation by introducing it into germ-free (GF) IL-10−/− mice.
Methods: GF IL-10−/− or WT mice were monoassociated with Bifidobacterium animalis subsp. animalis ATCC (American Type Culture Collection, Manassas, VA) 25527T or with B. infantis ATCC 15697T. Inflammation was measured by blinded histologic scores of the duodenum, cecum, and colon and by spontaneous secretion of IL-12/IL-23 p40 from colonic explants. Bacterial antigen-specific CD4+ mesenteric lymph node (MLN) T-cell recall responses were measured in response to antigen-presenting cells (APC) pulsed with bacterial lysates.
Results:B. animalis caused marked duodenal inflammation and mild colitis in monoassociated IL-10−/− mice, whereas the intestinal tracts of WT animals remained free of inflammation. B. infantis colonization resulted in mild inflammation in the duodena of IL-10−/− mice. CD4+ MLN T cells from B. animalis monoassociated IL-10−/− mice secreted high levels of IFN-γ and IL-17 in response to B. animalis lysate. B. animalis equally colonized the different intestinal regions of WT and IL-10−/− mice.
Conclusions:B. animalis, a traditional probiotic species that is expanded in experimental colitis in this model, induces marked duodenal and mild colonic inflammation and TH1/TH17 immune responses when introduced alone into GF IL-10−/− mice. This suggests a potential pathogenic role for this commensal bacterial species in a susceptible host.
(Inflamm Bowel Dis 2009)