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Limosilactobacillus johnsoni and Limosilactobacillus mucosae and Their Extracellular Vesicles Alleviate Gut Inflammatory Injury by Mediating Macrophage Polarization in a Lipopolysaccharide-Challenged Piglet Model

文献类型： 外文期刊

作者： Li, Jingjing;Feng, Shengkai;Pi, Yu;Jiang, Xianren;Li, Xilong;Zhou, Zutao;Liu, Xiangdong;Wei, Hong;Tao, Shiyu

作者机构：

关键词： intestinal epithelial cells;Limosilactobacillus johnsoni;Limosilactobacillus mucosae;macrophage;piglet model

期刊名称： JOURNAL OF NUTRITION

ISSN： 0022-3166

年卷期： 2023 年 153 卷 8 期

页码：

收录情况： SCIE（2023版）

摘要： Background: Limosilactobacillus johnsoni (L. j) and Limosilactobacillus mucosae (L. m) can alleviate the inflammatory response. Objectives: This study aimed to elucidate the underlying mechanisms by which L. j-and L. m-derived extracellular vesicles (EVs) mitigate lipopolysaccharide (LPS)-induced intestinal injury. Methods: Piglets were assigned to 4 groups: oral phosphate-buffered saline inoculation for 2 wk prior to intraperitoneal injection of physiological saline or LPS, and oral L. j/L. m inoculation for 2 wk prior to intraperitoneal injection of LPS. The intestinal integrity, macrophage markers, cytokine levels, and microbiota were determined. The cytokine levels and macrophage phenotype were detected after L. j/L. m and their EVs were coincubated with macrophages. The levels of cytokines, tight junction proteins, and apoptosis were measured after intestinal epithelial cells were cocultured with macrophages. Results: LPS challenge decreased jejunal villus length; expression levels of zonula occludens-1(ZO-1), occludin, arginase-1 (Arg1), and interleukin (IL)-10; and number of CD163 thorn cells and increased the expression levels of inducible nitric oxide synthase (iNOS), IL-1I3, IL-6, and tumor necrosis factor (TNF)-& alpha; compared with that in the control. L. j and L. m pretreatment rescued the aforementioned indicators compared with LPS challenge. Pretreatment of L. j and L. m and their EVs reversed the levels of IL-1I3, IL-6, TNF-& alpha;, and IL-10 and the gene expression of iNOS and Arg1 in the LPS group in macrophages. Pretreatment with L. j and L. m-derived EVs increased ZO-1 and occludin mRNA expression and reduced IL-1I3, caspase-3, and bax gene expression in intestinal epithelial cells of the coculture system. Enzyme-treated EVs were less effective than native EVs. Conclusions: This study suggests that EVs secreted by L. j and L. m control inflammation by modulating macrophage polarization, thereby improving intestinal barrier function.

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