Toll-like receptor 3 signaling drives enteric glial cells against dextran sulfate sodium-induced colitis in mice

IF 2.9 4区生物学 Q3 CELL BIOLOGY

Journal of Molecular Histology Pub Date : 2024-02-20 DOI:10.1007/s10735-024-10184-7

Jian Zeng, Qiong-Qiong Lu, Xiao-Long Du, Ling Yuan, Xiao-Jun Yang

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Abstract

The activation of toll-like receptor 3 (TLR3) has been reported to attenuate astrocytes injury in central nervous system, but its effect on enteric glial cells (EGCs) remains unknown. Here, we confirmed that the residence of EGCs was regulated by TLR3 agonist (polyinosinic-polycytidylic acid, PIC) or TLR3/dsRNA complex inhibitor in dextran sulfate sodium (DSS)-induced mice. In vitro, TLR3 signaling prevented apoptosis in EGCs and drove the secretion of EGCs-derived glial cell line-derived neurotrophic factor, 15-hydroxyeicosatetraenoic acid and S-nitrosoglutathione. PIC preconditioning enhanced the protective effects of EGCs against the dysfunction of intestinal epithelial barrier and the development of colitis in DSS-induced mice. Interestingly, PIC stimulation also promoted the effects of EGCs on converting macrophages to an M2-like phenotype and regulating the levels of inflammatory cytokines, including IL-1β, TNF-α and IL-10, in DSS-induced mice. These findings imply that TLR3 signaling in EGCs may provide a potential target for the prevention and treatment of colitis.

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Toll 样受体 3 信号驱动肠胶质细胞对抗葡聚糖硫酸钠诱导的小鼠结肠炎。

据报道，激活收费样受体3（TLR3）可减轻中枢神经系统中星形胶质细胞的损伤，但其对肠道胶质细胞（EGCs）的影响尚不清楚。在这里，我们证实在葡聚糖硫酸钠（DSS）诱导的小鼠体内，TLR3激动剂（聚肌苷酸-聚胞苷酸，PIC）或TLR3/dsRNA复合物抑制剂可调节EGCs的驻留。在体外，TLR3 信号可防止 EGCs 细胞凋亡，并促进 EGCs 衍生神经胶质细胞系营养因子、15-羟基二十碳四烯酸和 S-亚硝基谷胱甘肽的分泌。PIC预处理增强了EGCs对DSS诱导的小鼠肠上皮屏障功能障碍和结肠炎发展的保护作用。有趣的是，PIC刺激还能促进EGCs将巨噬细胞转化为M2样表型，并调节DSS诱导的小鼠体内炎症细胞因子（包括IL-1β、TNF-α和IL-10）的水平。这些研究结果表明，EGCs中的TLR3信号可能是预防和治疗结肠炎的潜在靶点。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Journal of Molecular Histology 生物-细胞生物学

CiteScore

5.90

自引率

0.00%

发文量

审稿时长

1 months

期刊介绍： The Journal of Molecular Histology publishes results of original research on the localization and expression of molecules in animal cells, tissues and organs. Coverage includes studies describing novel cellular or ultrastructural distributions of molecules which provide insight into biochemical or physiological function, development, histologic structure and disease processes. Major research themes of particular interest include: - Cell-Cell and Cell-Matrix Interactions; - Connective Tissues; - Development and Disease; - Neuroscience. Please note that the Journal of Molecular Histology does not consider manuscripts dealing with the application of immunological or other probes on non-standard laboratory animal models unless the results are clearly of significant and general biological importance. The Journal of Molecular Histology publishes full-length original research papers, review articles, short communications and letters to the editors. All manuscripts are typically reviewed by two independent referees. The Journal of Molecular Histology is a continuation of The Histochemical Journal.