Abstract
BackgroundInflammatory bowel disease (IBD) involves a breakdown in interactions between the host immune response and the resident commensal microbiota. Recent studies have suggested gut physiology and pathology relevant to human IBD can be rapidly modeled in zebrafish larvae. The aim of this study was to investigate the dysbiosis of intestinal microbiota in zebrafish models with IBD-like enterocolitis using culture-independent techniques.ResultsIBD-like enterocolitis was induced by exposing larval zebrafish to trinitrobenzenesulfonic acid (TNBS). Pathology was assessed by histology and immunofluorescence. Changes in intestinal microbiota were evaluated by denaturing gradient gel electrophoresis (DGGE) and the predominant bacterial composition was determined with DNA sequencing and BLAST and confirmed by real-time polymerase chain reaction. Larval zebrafish exposed to TNBS displayed intestinal-fold architecture disruption and inflammation reminiscent of human IBD. In this study, we defined a reduced biodiversity of gut bacterial community in TNBS-induced coliitis. The intestinal microbiota dysbiosis in zebrafish larvae with IBD-like colitis was characterized by an increased proportion of Proteobacteria (especially Burkholderia) and a decreased of Firmicutes(Lactobacillus group), which were significantly correlated with enterocolitis severity(Pearson correlation p < 0.01).ConclusionsThis is the first description of intestinal microbiota dysbiosis in zebrafish IBD-like models, and these changes correlate with TNBS-induced enterocolitis. Prevention or reversal of this dysbiosis may be a viable option for reducing the incidence and severity of human IBD.
Highlights
Inflammatory bowel disease (IBD) involves a breakdown in interactions between the host immune response and the resident commensal microbiota
Zebrafish collected at 4 dpf showed no significant difference between trinitrobenzenesulfonic acid (TNBS)-treated and control
Bacterial species associated with inflammatory disorder In order to define the key members of intestinal microbiota that likely contributed to the pathogenesis of TNBS-induced inflammatory disorder, we further identified the alteration of the dominant bacterial species in zebrafish gastrointestinal tract
Summary
Inflammatory bowel disease (IBD) involves a breakdown in interactions between the host immune response and the resident commensal microbiota. The aim of this study was to investigate the dysbiosis of intestinal microbiota in zebrafish models with IBD-like enterocolitis using culture-independent techniques. The precise etiology of IBD remains unclear, several factors are believed to play a role in its development and progression, including host genotype, immune disequilibrium, the composition of microbial communities resident in the GI tract and environmental factors [1,2]. IBD clearly involves a breakdown in interactions between the host immune response and the resident commensal microbiota. That the restoration of microbial diversity is effective suggests the intestinal microbiota alteration may play a key role in disease pathogenesis. Our knowledge of the microbiota shifts associated with IBD is far from complete, and it remains a question whether these changes are responsible for the origin of IBD, or alternatively, a direct or indirect consequence
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