Abstract
BackgroundCompelling evidences demonstrated that gut microbiota dysbiosis plays a critical role in the pathogenesis of inflammatory bowel diseases (IBD). Therapies for targeting the microbiota may provide alternative options for the treatment of IBD, such as probiotics. Here, we aimed to investigate the protective effect of a probiotic strain, Pediococcus pentosaceus (P. pentosaceus) CECT 8330, on dextran sulfate sodium (DSS)-induced colitis in mice.MethodsC57BL/6 mice were administered phosphate-buffered saline (PBS) or P. pentosaceus CECT 8330 (5 × 108 CFU/day) once daily by gavage for 5 days prior to or 2 days after colitis induction by DSS. Weight, fecal conditions, colon length and histopathological changes were examined. ELISA and flow cytometry were applied to determine the cytokines and regulatory T cells (Treg) ratio. Western blot was used to examine the tight junction proteins (TJP) in colonic tissues. Fecal short-chain fatty acids (SCFAs) levels and microbiota composition were analyzed by targeted metabolomics and 16S rRNA gene sequencing, respectively. The Kyoto Encyclopedia of Genes and Genomes (KEGG) and Cluster of orthologous groups of proteins (COG) pathway analysis were used to predict the microbial functional profiles.ResultsP. pentosaceus CECT 8330 treatment protected DSS-induced colitis in mice as evidenced by reducing the weight loss, disease activity index (DAI) score, histological damage, and colon length shortening. P. pentosaceus CECT 8330 decreased the serum levels of proinflammatory cytokines (TNF-α, IL-1β, and IL-6), and increased level of IL-10 in DSS treated mice. P. pentosaceus CECT 8330 upregulated the expression of ZO-1, Occludin and the ratio of Treg cells in colon tissue. P. pentosaceus CECT 8330 increased the fecal SCFAs level and relative abundances of several protective bacteria genera, including norank_f_Muribaculaceae, Lactobacillus, Bifidobacterium, and Dubosiella. Furthermore, the increased abundances of bacteria genera were positively correlated with IL-10 and SCFAs levels, and negatively associated with IL-6, IL-1β, and TNF-α, respectively. The KEGG and COG pathway analysis revealed that P. pentosaceus CECT 8330 could partially recover the metabolic pathways altered by DSS.ConclusionsP. pentosaceus CECT 8330 administration protects the DSS-induced colitis and modulates the gut microbial composition and function, immunological profiles, and the gut barrier function. Therefore, P. pentosaceus CECT 8330 may serve as a promising probiotic to ameliorate intestinal inflammation.
Highlights
Compelling evidences demonstrated that gut microbiota dysbiosis plays a critical role in the pathogenesis of inflammatory bowel diseases (IBD)
P. pentosaceus CECT 8330 protects dextran sulfate sodium (DSS)‐induced colitis To examine the protective effect of P. pentosaceus CECT 8330 on DSS-induced colitis in mice, we treated the mice with P. pentosaceus CECT 8330 prior to or 2 days after DSS administration for 5 days (Fig. 1A, Additional file 1: Fig. S1A)
The results revealed that the increased abundance of several genera by DSS were positively correlated with serum inflammatory cytokines (IL-6, IL-1β, and Tumor necrosis factor (TNF)-α) and negatively associated with IL-10, short-chain fatty acids (SCFAs), including Lachnospiraceae_NK4A136_group, norank_f_norank_o_Clostridia_UCG-014, Clostridium_sensu_stricto_1, Clostridia_vadinBB60_group, Oscillibacter, GCA_900066575, and norank_f_Ruminococcaceae
Summary
Compelling evidences demonstrated that gut microbiota dysbiosis plays a critical role in the pathogenesis of inflammatory bowel diseases (IBD). Therapies for targeting the microbiota may provide alternative options for the treatment of IBD, such as probiotics. Inflammatory bowel diseases (IBD) is a group of inflammatory disorders of the digestive tract that mainly characterized by chronic and relapsing inflammation of the gut mucosa [1]. Patients with IBD usually suffered lifelong episodes of remission and relapse that significantly impair their quality of life. It is assumed that IBD is occurring in genetically susceptible individuals with a dysregulated immune response towards gut microbiota, and under the influence of environmental factors [7]
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