To model inflammatory bowel disease, we assessed infection with Helicobacter 
hepaticus 3B1 (ATCC 51449) and a potential probiotic Lactobacillus reuteri (ATCC 
PTA-6475) in gnotobiotic B6.129P2-IL-10(tm1Cgn) (IL-10(-/-) ) mice. No 
typhlocolitis developed in germ-free controls (n=21) or in L. reuteri (n=8) or 
H. hepaticus (n=18) mono-associated mice for 20 weeks post-infection. As 
positive controls, three specific pathogen-free IL-10(-/-) mice dosed with H. 
hepaticus developed severe typhlocolitis within 11 weeks. Because L. reuteri 
PTA-6475 has anti-inflammatory properties in vitro, it was unexpected to observe 
significant typhlocolitis (P<0·0001) in mice that had been infected with L. 
reuteri followed in 1 week by H. hepaticus (n=16). The H. hepaticus colonization 
was not affected through 20 weeks post-infection but L. reuteri colonization was 
lower in co-infected compared with L. reuteri mono-associated mice at 8-11 weeks 
post-infection (P<0·05). Typhlocolitis was associated with an increased T helper 
type 1 serum IgG2c response to H. hepaticus in co-infected mice compared with H. 
hepaticus mono-associated mice (P<0·005) and similarly, mRNA expression in 
caecal-colonic tissue was elevated at least twofold for chemokine ligands and 
pro-inflammatory interleukin-1α (IL-1α), IL-1β, IL-12 receptor, tumour necrosis 
factor-α and inducible nitric oxide synthase. Anti-inflammatory transforming 
growth factor-β, lactotransferrin, peptidoglycan recognition proteins, Toll-like 
receptors 4, 6, 8 and particularly 9 gene expression, were also elevated only in 
co-infected mice (P<0·05). These data support that the development of 
typhlocolitis in H. hepaticus-infected IL-10(-/-) mice required co-colonization 
with other microbiota and in this study, required only L. reuteri. Although the 
effects other microbiota may have on H. hepaticus virulence properties remain 
speculative, further investigations using this gnotobiotic model are now 
possible.