Abstract
BackgroundDisturbances in the intestinal microbial community (i.e. dysbiosis) or presence of the microbes with deleterious effects on colonic mucosa has been linked to the pathogenesis of inflammatory bowel diseases. However the role of microbiota in induction and progression of ulcerative colitis (UC) has not yet been fully elucidated.MethodsThree lines of human microbiota-associated (HMA) mice were established by gavage of colon biopsy from three patients with active UC. The shift in microbial community during its transferring from humans to mice was analyzed by next-generation sequencing using Illumina MiSeq sequencer. Spontaneous or dextran sulfate sodium (DSS)-induced colitis and microbiota composition profiling in germ-free mice and HMA mice over 3–4 generations were assessed to decipher the features of the distinctive and crucial events occurring during microbial colonization and animal reproduction.ResultsNone of the HMA mice developed colitis spontaneously. When treated with DSS, mice in F4 generation of one line of colonized mice (aHMA) developed colitis. Compared to the DSS-resistant earlier generations of aHMA mice, the F4 generation have increased abundance of Clostridium difficile and decrease abundance of C. symbiosum in their cecum contents measured by denaturing gradient gel electrophoresis and DNA sequencing.ConclusionIn our study, mucosa-associated microbes of UC patients were not able to induce spontaneous colitis in gnotobiotic BALB/c mice but they were able to increase the susceptibility to DSS-induced colitis, once the potentially deleterious microbes found a suitable niche.Electronic supplementary materialThe online version of this article (doi:10.1186/s13099-015-0080-2) contains supplementary material, which is available to authorized users.
Highlights
Disturbances in the intestinal microbial community or presence of the microbes with deleterious effects on colonic mucosa has been linked to the pathogenesis of inflammatory bowel diseases
This suggests that abundances of major bacterial taxa are similar among all three biopsy samples and low abundance species contributed to the difference between biopsy b and biopsy a or biopsy c
The diversity of microbiota is decreased after the colonization GF mice were successfully colonized with bacteria from biopsies of three patients with active ulcerative colitis (UC) (Fig. 1a, c)
Summary
Disturbances in the intestinal microbial community (i.e. dysbiosis) or presence of the microbes with deleterious effects on colonic mucosa has been linked to the pathogenesis of inflammatory bowel diseases. Crohn’s disease (CD) and ulcerative colitis (UC), the two major types of inflammatory bowel disease (IBD), are characterized by chronic relapsing inflammation of the gastrointestinal tract. This inflammation is a result of an aberrant immune response to antigens of resident gut microbiota [1, 2]. The gut microbiota ecology in UC patients is significantly different from the microbiota in healthy subjects, with typical reduction of diversity among major anaerobic species [6,7,8] Transfer of this luminal dysbiotic microbial community to the germ-free mice renders them more susceptible to experimentally-induced intestinal inflammation than similar transfer from healthy subjects [9]. Due to the close contact with gut mucosa, the adherent microbes may be even more important
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