Pediococcus pentosaceus CECT 8330 protects DSS-induced colitis and regulates the intestinal microbiota and immune responses in mice.
Pediococcus pentosaceus CECT 8330 protects DSS-induced colitis and regulates the intestinal microbiota and immune responses in mice.
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戊糖片球菌 CECT 8330 保护 DSS 诱导的结肠炎并调节小鼠肠道微生物群和免疫反应
DOI：
10.1186/s12967-022-03235-8
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发表时间：
2022-01-15
影响因子：
7.4
通讯作者：
Wang Y
中科院分区：
文献类型：
--
作者：
Dong F;Xiao F;Li X;Li Y;Wang X;Yu G;Zhang T;Wang Y
令人信服的证据表明，肠道微生物群失调在炎症性肠病（IBD）的发病机制中起着关键作用。靶向微生物群的疗法可以为IBD的治疗提供替代选择，例如益生菌。在这里，我们旨在研究益生菌菌株戊糖片球菌（P. pentosaceus）CECT 8330对葡聚糖硫酸钠（DSS）诱导的小鼠结肠炎的保护作用。在DSS诱导结肠炎前5天或诱导结肠炎后2天，每天一次灌胃给予C57 BL/6小鼠磷酸盐缓冲盐水（PBS）或戊糖毕赤酵母CECT 8330（5 × 108 CFU/天）。检查体重、粪便状况、结肠长度和组织病理学变化。采用ELISA和流式细胞术检测细胞因子和调节性T细胞（Treg）的比例。Western blot检测结肠组织中紧密连接蛋白（TJP）的表达。分别通过靶向代谢组学和16 S rRNA基因测序分析粪便短链脂肪酸（SCFAs）水平和微生物群组成。利用京都基因和基因组百科全书（KEGG）和邻位同源蛋白组簇（COG）途径分析预测微生物功能谱。戊糖毕赤酵母CECT 8330处理保护DSS诱导的小鼠结肠炎，如通过减少体重减轻、疾病活动指数（DAI）评分、组织学损伤和结肠长度缩短所证明的。戊糖青霉CECT 8330降低DSS处理的小鼠中促炎细胞因子（TNF-α、IL-1β和IL-6）的血清水平，并增加IL-10的水平。戊糖青霉CECT 8330可上调结肠组织ZO-1、Occludin的表达及Treg细胞比例。戊糖毕赤酵母CECT 8330增加粪便SCFAs水平和几种保护性细菌属的相对丰度，所述保护性细菌属包括野杆菌科、乳杆菌属、双歧杆菌属和杜氏杆菌属。此外，细菌属的丰度增加与IL-10和SCFAs水平呈正相关，与IL-6、IL-1β和TNF-α分别呈负相关。KEGG和COG途径分析表明，戊糖毕赤酵母CECT 8330可以部分恢复DSS改变的代谢途径。戊糖毕赤酵母CECT 8330施用保护DSS诱导的结肠炎并调节肠道微生物组成和功能、免疫学特征和肠道屏障功能。因此，戊糖毕赤酵母CECT 8330可能作为一种有前途的益生菌，以改善肠道炎症。在线版本包含补充材料，可通过10.1186/s12967-022-03235-8获取。
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. 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. C57BL/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. P. 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. P. 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. The online version contains supplementary material available at 10.1186/s12967-022-03235-8.
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影响因子：
3.9
作者：
Cui G;Yuan A
通讯作者：
Yuan A
影响因子：
32.4
作者：
Dorrestein PC;Mazmanian SK;Knight R
通讯作者：
Knight R
影响因子：
3.1
作者：
Alizadeh, Arash;Akbari, Peyman;Garssen, Johan;Fink-Gremmels, Johanna;Braber, Saskia
通讯作者：
Braber, Saskia
影响因子：
24.5
作者：
Kruis, W;Fric, P;Schulze, J
通讯作者：
Schulze, J
影响因子：
2.4
作者：
Bosch, M.;Rodriguez, M.;Cune, J.
通讯作者：
Cune, J.