No Cover Image

Journal article 761 views 368 downloads

Endometrial cells sense and react to tissue damage during infection of the bovine endometrium via interleukin 1 / Laura, Healy; James, Cronin; Martin, Sheldon

Scientific Reports, Volume: 4, Start page: 7060

Swansea University Authors: Laura, Healy, James, Cronin, Martin, Sheldon

  • srep07060.pdf

    PDF | Version of Record

    Distributed under the terms of a Creative Commons Attribution (CC-BY-4.0)

    Download (576.71KB)

DOI (Published version): 10.1038/srep07060

Abstract

Cells generate inflammatory responses to bacteria when pattern recognition receptors bind pathogen-associated molecules such as lipopolysaccharide. Cells may also respond to tissue damage by sensing damage-associated molecules. Postpartum bacterial infections of the bovine uterus cause endometritis...

Full description

Published in: Scientific Reports
Published: 2014
URI: https://cronfa.swan.ac.uk/Record/cronfa19258
Tags: Add Tag
No Tags, Be the first to tag this record!
Abstract: Cells generate inflammatory responses to bacteria when pattern recognition receptors bind pathogen-associated molecules such as lipopolysaccharide. Cells may also respond to tissue damage by sensing damage-associated molecules. Postpartum bacterial infections of the bovine uterus cause endometritis but the risk of disease is increased by tissue trauma triggered by dystocia. Animals that suffered dystocia had increased concentrations of inflammatory mediators IL-8, IL-1β and IL-1α in vaginal mucus 3 weeks postpartum, but they also had more bacteria than normal animals. Ex vivo organ cultures of endometrium, endometrial cells and peripheral blood monocytes did not generate inflammatory responses to prototypical damage molecules, HMGB1 or hyaluronan, or to necrotic cells; although they secreted IL-6 and IL-8 in a concentration-dependent manner when treated with IL-1α. However, necrotic endometrial cells did not accumulate intracellular IL-1α or release IL-1α, except when pre-treated with lipopolysaccharide or bacteria. Endometrial cell inflammatory responses to IL-1α were dependent on the cognate receptor IL-1R1, and the receptor adaptor protein MyD88, and the inflammatory response to IL-1α was independent of the response to lipopolysaccharide. Rather than a typical damage-associated molecule, IL-1α acts to scale the inflammatory response in recognition that there is a combination of pathogen challenge followed by endometrial cell damage.
Item Description: This work was funded by Sheldon's UK Biotechnology and Biological Sciences Research Council grant (BBSRC, grant F005121/1).Healy was a PhD student supervised by Sheldon.
Start Page: 7060