Abstract
Flavonifractor plautii (FP) has been reported to participate in the metabolism of catechins in the human gut. However, there is limited information on the immune regulatory effects of this bacterium. We confirmed that the administration of green tea increases the abundance of FP in the gut microbiota and investigated the effect of FP in a mouse colitis model. Mice were orally administered FP for 10 consecutive days; colonic inflammation was evaluated daily on the basis of stool consistency, gross rectal bleeding, and body weight. In the dextran sodium sulfate model, FP-exposed animals exhibited lower levels of inflammation and strong inhibition of interleukin (IL)-17 signaling. Moreover, lipoteichoic acid from FP was identified as the active component mediating IL-17 suppression. Thus, oral administration of FP appears to modulate gut inflammation and represents a viable and inexpensive oral microbial therapeutic.
Highlights
Inflammatory bowel disease (IBD) is a generic term for chronic inflammatory disease in the gastrointestinal tract, typified by Crohn’s disease and ulcerative colitis [1]
Flavonifractor plautii (FP) was cultured in Gifu Anaerobic Medium (GAM) broth (Nissui Pharmaceutical Co., Ltd., Tokyo, Japan), and the cells were pelleted by centrifugation at 8,000 × g, 4◦C for 5 min, and washed with and resuspended in sterile water to yield a suspension at a density of 1 × 1011 colony-forming units/mL
The relative abundance of FP in feces was higher in the green tea supplementation group on day 8 (Figure 1F)
Summary
Inflammatory bowel disease (IBD) is a generic term for chronic inflammatory disease in the gastrointestinal tract, typified by Crohn’s disease and ulcerative colitis [1]. IBD patients exhibit macrophage infiltration and excessive activation of tumor necrosis factor alpha (TNF-α) and interleukin (IL)-17 in local inflammation [2]. This results in tissue injury, such as intestinal barrier disruption and ulceration [3], and the development of further hyperimmunity [4]. In the last 30 years, the number of IBD patients has been rapidly increasing, mainly in Europe and the United States, and a similar trend in Japan has been observed [9, 10]. A genetic predisposition and the involvement of environmental factors have been reported in the development of IBD [11, 12].
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