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Endometrial cells sense and react to tissue damage during infection of the bovine endometrium via interleukin 1

Laura Healy Orcid Logo, James Cronin Orcid Logo, I. Martin Sheldon, Martin Sheldon Orcid Logo

Scientific Reports, Volume: 4, Start page: 7060

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

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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...

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Published in: Scientific Reports
Published: 2014
URI: https://cronfa.swan.ac.uk/Record/cronfa19258
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spelling 2019-09-02T15:54:07.1566275 v2 19258 2014-11-14 Endometrial cells sense and react to tissue damage during infection of the bovine endometrium via interleukin 1 2a2ece586118255cd972a63b78cf8ea3 0000-0003-2241-7512 Laura Healy Laura Healy true false 9cfd17551c0d1f7438895121e4fbb6e8 0000-0002-0590-9462 James Cronin James Cronin true false ab0f74b794e59cc270c69e63ee1d9748 0000-0001-7902-5558 Martin Sheldon Martin Sheldon true false 2014-11-14 FGMHL 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. Journal Article Scientific Reports 4 7060 14 11 2014 2014-11-14 10.1038/srep07060 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. COLLEGE NANME Medicine, Health and Life Science - Faculty COLLEGE CODE FGMHL Swansea University BBSRC 2019-09-02T15:54:07.1566275 2014-11-14T14:41:20.7345987 Laura Healy 0000-0003-2241-7512 1 James Cronin 0000-0002-0590-9462 2 I. Martin Sheldon 3 Martin Sheldon 0000-0001-7902-5558 4 0019258-29032015215246.pdf srep07060.pdf 2015-03-29T21:52:46.9830000 Output 567823 application/pdf Version of Record true 2014-11-14T00:00:00.0000000 Distributed under the terms of a Creative Commons Attribution (CC-BY-4.0) true
title Endometrial cells sense and react to tissue damage during infection of the bovine endometrium via interleukin 1
spellingShingle Endometrial cells sense and react to tissue damage during infection of the bovine endometrium via interleukin 1
Laura Healy
James Cronin
Martin Sheldon
title_short Endometrial cells sense and react to tissue damage during infection of the bovine endometrium via interleukin 1
title_full Endometrial cells sense and react to tissue damage during infection of the bovine endometrium via interleukin 1
title_fullStr Endometrial cells sense and react to tissue damage during infection of the bovine endometrium via interleukin 1
title_full_unstemmed Endometrial cells sense and react to tissue damage during infection of the bovine endometrium via interleukin 1
title_sort Endometrial cells sense and react to tissue damage during infection of the bovine endometrium via interleukin 1
author_id_str_mv 2a2ece586118255cd972a63b78cf8ea3
9cfd17551c0d1f7438895121e4fbb6e8
ab0f74b794e59cc270c69e63ee1d9748
author_id_fullname_str_mv 2a2ece586118255cd972a63b78cf8ea3_***_Laura Healy
9cfd17551c0d1f7438895121e4fbb6e8_***_James Cronin
ab0f74b794e59cc270c69e63ee1d9748_***_Martin Sheldon
author Laura Healy
James Cronin
Martin Sheldon
author2 Laura Healy
James Cronin
I. Martin Sheldon
Martin Sheldon
format Journal article
container_title Scientific Reports
container_volume 4
container_start_page 7060
publishDate 2014
institution Swansea University
doi_str_mv 10.1038/srep07060
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description 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.
published_date 2014-11-14T03:22:34Z
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