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

Autor: Zeng J; Department of Gastroenterology, Chongqing Hospital of Traditional Chinese Medicine, Chongqing, China. zengjianhuaxi@163.com., Lu QQ; Department of Gastroenterology, Chongqing Hospital of Traditional Chinese Medicine, Chongqing, China., Du XL; Department of Gastroenterology, Chongqing Hospital of Traditional Chinese Medicine, Chongqing, China., Yuan L; Department of Gastroenterology, Chongqing Hospital of Traditional Chinese Medicine, Chongqing, China., Yang XJ; Department of Gastroenterology, Chongqing Hospital of Traditional Chinese Medicine, Chongqing, China.
Jazyk: angličtina
Zdroj: Journal of molecular histology [J Mol Histol] 2024 Apr; Vol. 55 (2), pp. 201-210. Date of Electronic Publication: 2024 Feb 20.
DOI: 10.1007/s10735-024-10184-7
Abstrakt: 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.
(© 2024. The Author(s), under exclusive licence to Springer Nature B.V.)
Databáze: MEDLINE
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