Abstract

Disturbed balance between microbiota, epithelial cells, and resident immune cells within the intestine contributes to inflammatory bowel disease (IBD) pathogenesis. The Citrobacter rodentium-induced colitis mouse model has been well documented. This model allows the analysis of host responses to enteric bacteria and facilitates improved understanding of the potential mechanisms of IBD pathogenesis. The current study evaluated the effects of dietary 30 mg/kg quercetin supplementation on C. rodentium-induced experimental colitis in C57BL/6 mice. Following dietary quercetin supplementation, the mice were infected with 5 × 108 CFU C. rodentium, and the pathological effects of C. rodentium were measured. The results showed that quercetin alleviated the effects of C. rodentium-induced colitis, suppressed the production of pro-inflammatory cytokines, such as interleukin (IL)-17, tumor necrosis factor alpha, and IL-6 (p < 0.05), and promoted the production of IL-10 in the colon tissues (p < 0.05). Quercetin supplementation also enhanced the populations of Bacteroides, Bifidobacterium, Lactobacillus, and Clostridia and significantly reduced those of Fusobacterium and Enterococcus (p < 0.05). These findings indicate that dietary quercetin exerts therapeutic effects on C. rodentium-induced colitis, probably due to quercetin’s ability to suppress pro-inflammatory cytokines and/or modify gut microbiota. Thus, these results suggest that quercetin supplementation is effective in controlling C. rodentium-induced inflammation.

Highlights

  • In the last decade, inflammatory bowel disease (IBD) has been one of the most frequently investigated human health issues associated with the gut microbiota (Kostic et al, 2014)

  • These symbiotic inhabitants, collectively known as the gut microbiota, supply vital nutrients and limit the colonization of pathogenic microbes in the gut (Honda and Takeda, 2009). Evidence from both IBD patients and mouse models has shown that profound changes in the gut, such as intestinal microbiota development, play a major role in IBD pathogenesis (Gkouskou et al, 2014; Matsuoka and Kanai, 2015)

  • Similar to enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC), Citrobacter rodentium is a member of the noninvasive group of attaching and effacing (A/E) bacteria that attach themselves to the intestinal epithelium and colonizes the host’s gut

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Summary

Introduction

Inflammatory bowel disease (IBD) has been one of the most frequently investigated human health issues associated with the gut microbiota (Kostic et al, 2014). The intestinal tract contains 10 trillion microorganisms (Dave et al, 2012) that are separated from the host’s mucosal immune cells by single layer of polarized epithelial cells play a crucial role in the development of the mucosal immune system These symbiotic inhabitants, collectively known as the gut microbiota, supply vital nutrients and limit the colonization of pathogenic microbes in the gut (Honda and Takeda, 2009). Similar to enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC), Citrobacter rodentium is a member of the noninvasive group of attaching and effacing (A/E) bacteria that attach themselves to the intestinal epithelium and colonizes the host’s gut At this point, the A/E pathogens induce alterations in the colonic tissue similar to those observed in cases of EPEC or EHEC infections in murine and human IBD (Law et al, 2013). Research related to C. rodentium is a key step for developing innovative prophylactic and therapeutic treatments

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