Research Library

Premium Expression and function of macrophage‐inducible C‐type lectin (Mincle) in inflammation driven parturition in fetal membranes and myometrium
Author(s)
Lim R.,
Lappas M.
Publication year2019
Publication title
clinical & experimental immunology
Resource typeJournals
PublisherWiley-Blackwell
Summary The pivotal role of inflammatory processes in human parturition is well known, but not completely understood. We have performed a study to examine the role of macrophage‐inducible C‐type lectin (Mincle) in inflammation‐associated parturition. Using human samples, we show that spontaneous labour is associated with up‐regulated Mincle expression in the myometrium and fetal membranes. Mincle expression was also increased in fetal membranes and myometrium in the presence of pro‐labour mediators, the proinflammatory cytokines interleukin (IL)‐1B and tumour necrosis factor (TNF), and Toll‐like receptor (TLR) ligands fsl‐1, poly(I:C), lipopolysaccharide (LPS) and flagellin. These clinical studies are supported by mouse studies, where an inflammatory challenge in a mouse model of preterm birth increased Mincle expression in the uterus. Importantly, elimination of Mincle decreased the effectiveness of proinflammatory cytokines and TLR ligands to induce the expression of pro‐labour mediators; namely, proinflammatory cytokines and chemokines, contraction‐associated proteins and prostaglandins, and extracellular matrix remodelling enzymes, matrix metalloproteinases. The data presented in this study suggest that Mincle is required when inflammatory activation precipitates parturition.
Subject(s)biology , chemokine , endocrinology , immunology , inflammation , lipopolysaccharide , microbiology and biotechnology , myometrium , proinflammatory cytokine , tumor necrosis factor alpha , uterus
Language(s)English
eISSN1365-2249
pISSN0009-9104
DOI10.1111/cei.13281

Seeing content that should not be on Zendy? Contact us.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here