Enterococcus faecalis induces inflammatory bowel disease in interleukin-10 knockout mice - PubMed (original) (raw)
Enterococcus faecalis induces inflammatory bowel disease in interleukin-10 knockout mice
Edward Balish et al. Am J Pathol. 2002 Jun.
Abstract
Germ-free interleukin-10 knockout (IL-10 KO) mice developed inflammatory bowel disease (IBD) after they were colonized with a pure culture of Enterococcus faecalis. E. faecalis not only induced IBD (primarily in colon and rectum) but rectal dysplasia and adenocarcinoma was also found in the IL-10 KO mice. Conventional (complex-intestinal flora) IL-10 KO mice developed IBD within 10 to 15 weeks of age and showed more pathology in the cecum (typhlitis) than we observed with E. faecalis-induced IBD in gnotobiotic IL-10 KO mice. Conversely, neither germ-free IL-10 mice nor IL-10 KO mice colonized as adults, with a pure culture of Candida albicans, Escherichia coli, Lactobacillus casei, L. reuteri, L. acidophilus, a Bifidobacterium sp., Lactococcus lactis, or a Bacillus sp. developed IBD during the 25- to 30-week study. E. faecalis is a common intestinal microbe of man and animals that can trigger IBD, dysplasia, and carcinoma in a genetically susceptible murine host.
Figures
Figure 1.
Fissure (arrowhead) in cecum of IL-10−/− mouse infected with E. faecalis for 20 weeks. H&E; original magnification, ×100.
Figure 2.
Cryptabscesses (arrowheads) and loss of mucosal goblet cells in rectal mucosa of IL-10−/− mouse infected with E. faecalis for 10 weeks. H&E; original magnification, ×100.
Figure 3.
Normal rectal mucosa from an IL-10−/− germ-free mouse at age 21 weeks. H&E; original magnification, ×100.
Figure 4.
Extra-rectal extension of invasive adenocarcinoma showing dilated mucin-filled acini. IL-10−/− mouse infected with E. faecalis for 24 weeks. H&E; original magnification, ×100.
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