Expression and function of macrophage-inducible C-type lectin (Mincle) in inflammation driven parturition in fetal membranes and myometrium.

Publisher: Oxford University Press Country of Publication: England NLM ID: 0057202 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1365-2249 (Electronic) Linking ISSN: 00099104 NLM ISO Abbreviation: Clin Exp Immunol Subsets: MEDLINE

Publication: 2022- : Oxford : Oxford University Press
Original Publication: Oxford : Blackwell Scientific Publications

Extraembryonic Membranes/*immunology ; Lectins, C-Type/*immunology ; Myometrium/*immunology ; Parturition/*immunology ; Receptors, Immunologic/*immunology; Animals ; Chemokines/metabolism ; Cytokines/metabolism ; Extracellular Matrix/enzymology ; Extraembryonic Membranes/cytology ; Extraembryonic Membranes/metabolism ; Female ; Gene Knockdown Techniques ; Humans ; In Vitro Techniques ; Inflammation Mediators/metabolism ; Lectins, C-Type/antagonists & inhibitors ; Lectins, C-Type/genetics ; Membrane Proteins/genetics ; Membrane Proteins/immunology ; Mice ; Myometrium/cytology ; Myometrium/metabolism ; Parturition/genetics ; Parturition/metabolism ; Pregnancy ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Receptors, Immunologic/antagonists & inhibitors ; Receptors, Immunologic/genetics ; Receptors, Pattern Recognition/metabolism ; Up-Regulation

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.
(© 2019 British Society for Immunology.)

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Keywords: Mincle; fetal membranes; human labour; inflammation; myometrium

0 (CLEC4D protein, human)
0 (Chemokines)
0 (Clecsf8 protein, mouse)
0 (Cytokines)
0 (Inflammation Mediators)
0 (Lectins, C-Type)
0 (Membrane Proteins)
0 (RNA, Messenger)
0 (Receptors, Immunologic)
0 (Receptors, Pattern Recognition)

Date Created: 20190223 Date Completed: 20200406 Latest Revision: 20200701

20240829

PMC6591154

10.1111/cei.13281

30793298