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约氏乳杆菌GLJ001通过肠道微生物群-短链脂肪酸轴抑制M1巨噬细胞极化,从而预防小鼠DSS诱导的结肠炎。

Lactobacillus johnsonii GLJ001 prevents DSS-induced colitis in mice by inhibiting M1 macrophage polarization via gut microbiota-SCFAs axis.

作者信息

Cai Yunjie, Huang Yina, Wang Yu, Lin Cuiyao, Qiu Liang, Wei Hua

机构信息

State Key Laboratory of Food Science and Resources, Nanchang University, Nanchang, Jiangxi 330047, People's Republic of China.

College of Biological and Food Engineering, Anhui Polytechnic University, Wuhu, Anhui 241000, People's Republic of China.

出版信息

Int Immunopharmacol. 2025 Jan 10;144:113671. doi: 10.1016/j.intimp.2024.113671. Epub 2024 Nov 29.

DOI:10.1016/j.intimp.2024.113671
PMID:39615110
Abstract

Inflammatory Bowel Disease (IBD) is increasing worldwide and has become a global emergent disease. Probiotics have been reported to be effective in relieving colitis. Previous studies found ripened Pu-erh tea (RPT) promoted gut microbiota resilience against dextran sulfate sodium (DSS)-induced colitis in mice by increasing relative abundance of Lactobacillus. However, whether and how it alleviated DSS-induced colitis in mice need to be explored. Here, we screened a probiotic Lactobacillus johnsonii GLJ001 from feces of ripened Pu-erh tea (RPT)-administrated mice. In this study, L. johnsonii GLJ001 attenuated symptoms of DSS-induced colitis in mice, including weight loss, increased disease activity index (DAI), colon shortening and colon tissue damage, as well as high expression of inflammatory cytokines and disturbances of intestine barrier function. Furthermore, abundances of short-chain fatty acids (SCFAs)-producing bacteria (i.e. Clostridium cluster IV and XIVa, Lachnospiracea_incertae_sedis and Ruminococcus) were enhanced in the cecum of mice treated with L. johnsonii GLJ001, accompanying by an increase of SCFAs. It was also found that SCFAs inhibited mRNA expression of M1 macrophage markers (Inos and CD86), inflammatory cytokines (TNF-α and Il-1β) and SCFAs receptors (Gpr41 and Gpr43) induced by lipopolysaccharide (LPS) and interferon-γ (IFN-γ) in THP-1 cell line. Collectively, L. johnsonii GLJ001 prevented DSS-induced colitis in mice by inhibiting M1 macrophage polarization via gut microbiota-SCFAs axis, and can be administered for management of colitis.

摘要

炎症性肠病(IBD)在全球范围内呈上升趋势,已成为一种全球性的突发疾病。据报道,益生菌对缓解结肠炎有效。先前的研究发现,熟普洱茶(RPT)通过增加乳酸杆菌的相对丰度,促进肠道微生物群对葡聚糖硫酸钠(DSS)诱导的小鼠结肠炎的恢复力。然而,它是否以及如何减轻小鼠DSS诱导的结肠炎尚需探索。在此,我们从饮用熟普洱茶(RPT)的小鼠粪便中筛选出一种益生菌约氏乳杆菌GLJ001。在本研究中,约氏乳杆菌GLJ001减轻了小鼠DSS诱导的结肠炎症状,包括体重减轻、疾病活动指数(DAI)增加、结肠缩短和结肠组织损伤,以及炎症细胞因子的高表达和肠屏障功能紊乱。此外,在用约氏乳杆菌GLJ001处理的小鼠盲肠中,产生短链脂肪酸(SCFAs)的细菌(即梭菌属IV和XIVa簇、毛螺菌科未确定属和瘤胃球菌)的丰度增加,同时SCFAs也增加。还发现,SCFAs抑制脂多糖(LPS)和干扰素-γ(IFN-γ)在THP-1细胞系中诱导的M1巨噬细胞标志物(Inos和CD86)、炎症细胞因子(TNF-α和Il-1β)和SCFAs受体(Gpr41和Gpr43)的mRNA表达。总的来说,约氏乳杆菌GLJ001通过肠道微生物群-SCFAs轴抑制M1巨噬细胞极化,预防小鼠DSS诱导的结肠炎,可用于结肠炎的治疗。

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