Abstract
Treatment with the probiotic bacterium Lactobacillus reuteri has been shown to prevent dextran sodium sulfate (DSS)-induced colitis in rats. This is partly due to reduced P-selectin-dependent leukocyte- and platelet-endothelial cell interactions, however, the mechanism behind this protective effect is still unknown. In the present study a combination of culture dependent and molecular based T-RFLP profiling was used to investigate the influence of L. reuteri on the colonic mucosal barrier of DSS treated rats. It was first demonstrated that the two colonic mucus layers of control animals had different bacterial community composition and that fewer bacteria resided in the firmly adherent layer. During DSS induced colitis, the number of bacteria in the inner firmly adherent mucus layer increased and bacterial composition of the two layers no longer differed. In addition, induction of colitis dramatically altered the microbial composition in both firmly and loosely adherent mucus layers. Despite protecting against colitis, treatment with L. reuteri did not improve the integrity of the mucus layer or prevent distortion of the mucus microbiota caused by DSS. However, L. reuteri decreased the bacterial translocation from the intestine to mesenteric lymph nodes during DSS treatment, which might be an important part of the mechanisms by which L. reuteri ameliorates DSS induced colitis.
Highlights
Inflammatory bowel diseases (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), are multifactorial diseases, dependent on host genetics, environment, immune response and the intestinal microbiota
By culturing samples of the different colonic mucus layers under anaerobic conditions, we found that the total number of bacteria was significantly higher in the loosely adherent layer than in the firmly adherent layer in untreated and L. reuteri treated rats (Figure 2)
The constitution of the bacterial communities differed in the two colonic mucus layers, and fewer bacteria were found in the firmly adherent mucus
Summary
Inflammatory bowel diseases (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), are multifactorial diseases, dependent on host genetics, environment, immune response and the intestinal microbiota. During non-inflammatory conditions, the intestinal microbiota-host relationship is symbiotic, and the defense mechanisms preventing translocation of intestinal bacteria through the mucosa and concomitant immune activation are most likely tightly controlled. These mechanisms have been shown to include a luminal firmly adherent mucus layer as well as loosely adherent mucus [2,3,4], in addition to epithelial tight junctions and epithelial secretion of antibacterial peptides [5,6]. Secretion of the firmly adherent mucus has been shown to be stimulated by bacterial products through toll-like receptor signaling, underpinning the symbiotic relationship between host and intestinal microbiota [3]. A recent study has showed that the inner firm layer is devoid of or contain very low numbers of bacteria under noninflammatory conditions [4]
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