Abstract
This study aimed at determining the beneficial effect of Clostridium butyricum (CB) RH2 on ceftriaxone-induced dysbacteriosis. To this purpose, BALB/c mice were exposed to ceftriaxone (400 mg/ml) or not (control) for 7 days, and administered a daily oral gavage of low-, and high-dose CB RH2 (108 and 1010 CFU/ml, respectively) for 2 weeks. CB RH2 altered the diversity of gut microbiota, changed the composition of gut microbiota in phylum and genus level, decreased the F/B ratio, and decreased the pro-inflammatory bacteria (Deferribacteres, Oscillibacter, Desulfovibrio, Mucispirillum and Parabacteroides) in ceftriaxone-treated mice. Additionally, CB RH2 improved colonic architecture and intestinal integrity by improving the mucous layer and the tight junction barrier. Furthermore, CB RH2 also mitigated intestinal inflammation through decreasing proinflammatory factors (TNF-α and COX-2) and increasing anti-inflammatory factors (IL-10). CB RH2 had direct effects on the expansion of CD4+ T cells in Peyer’s patches (PPs) in vitro, which in turn affected their immune response upon challenge with ceftriaxone. All these data suggested that CB RH2 possessed the ability to modulate the intestinal mucosal and systemic immune system in limiting intestinal alterations to relieve ceftriaxone-induced dysbacteriosis.
Highlights
The intestine is different from the other organs of the human body because it consists of a physical and immunological protective barrier against foreign antigens and pathogens (Curciarello et al, 2019; Liang et al, 2020)
Results showed a strong clustering of the gut microbiota composition for each group, which suggested that high concentration of Clostridium butyricum (CB) RH2 made a certain impact on the gut microbiota composition of the ceftriaxone treated mice
To address whether supplementation of CB RH2 could suppress colon inflammation, we investigate the level of mRNA expression of proinflammatory factors, including tumor necrosis factor alpha (TNF-a) and cyclooxygenase-2 (COX-2)
Summary
The intestine is different from the other organs of the human body because it consists of a physical and immunological protective barrier against foreign antigens and pathogens (Curciarello et al, 2019; Liang et al, 2020). The gut microbiota has CB RH2 in Intestinal Dysbiosis diverse effects on the regulation of many various physiological processes, including nutrient digestion and acquisition, modulation of the gut-specific immune system, and protection from infectious pathogens (Wang et al, 2019). Growing evidences have demonstrated that the interplay between the gut microbiota, the intestinal barrier and the mucosal immune system is profoundly altered in multifarious diseases, such as cardiovascular disease (Lewis and Taylor, 2020), infectious disease (Rosel-Pech et al, 2020), inflammatory bowel disease (Lee et al, 2020), autoimmune disease (Antonini et al, 2019), and a variety of cancers (Yoo et al, 2020). Ceftriaxone, a b-lactam antibiotic, has high biliary elimination, which may result in a pronounced impact on the intestinal microbiota (Burdet et al, 2019). It was shown that ceftriaxoneinduced dysbiosis impacted the integrity of mucosal epithelial layer, which were accompanied by overexpression of mucin-2 (MUC-2) and overproduction of defensins and inflammatory cytokines (Li et al, 2015)
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