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Blocking LFA-1 Aggravates Cardiac Inflammation in Experimental Autoimmune Myocarditis
The lymphocyte function-associated antigen 1 (LFA-1) is a member of the beta2-integrin family and plays a pivotal role for T cell activation and leukocyte trafficking under inflammatory conditions. Blocking LFA-1 has reduced or aggravated inflammation depending on the inflammation model. To investig...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6830329/ https://www.ncbi.nlm.nih.gov/pubmed/31627327 http://dx.doi.org/10.3390/cells8101267 |
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author | Weckbach, Ludwig T. Uhl, Andreas Boehm, Felicitas Seitelberger, Valentina Huber, Bruno C. Kania, Gabriela Brunner, Stefan Grabmaier, Ulrich |
author_facet | Weckbach, Ludwig T. Uhl, Andreas Boehm, Felicitas Seitelberger, Valentina Huber, Bruno C. Kania, Gabriela Brunner, Stefan Grabmaier, Ulrich |
author_sort | Weckbach, Ludwig T. |
collection | PubMed |
description | The lymphocyte function-associated antigen 1 (LFA-1) is a member of the beta2-integrin family and plays a pivotal role for T cell activation and leukocyte trafficking under inflammatory conditions. Blocking LFA-1 has reduced or aggravated inflammation depending on the inflammation model. To investigate the effect of LFA-1 in myocarditis, mice with experimental autoimmune myocarditis (EAM) were treated with a function blocking anti-LFA-1 antibody from day 1 of disease until day 21, the peak of inflammation. Cardiac inflammation was evaluated by measuring infiltration of leukocytes into the inflamed cardiac tissue using histology and flow cytometry and was assessed by analysis of the heart weight/body weight ratio. LFA-1 antibody treatment severely enhanced leukocyte infiltration, in particular infiltration of CD11b+ monocytes, F4/80+ macrophages, CD4+ T cells, Ly6G+ neutrophils, and CD133+ progenitor cells at peak of inflammation which was accompanied by an increased heart weight/body weight ratio. Thus, blocking LFA-1 starting at the time of immunization severely aggravated acute cardiac inflammation in the EAM model. |
format | Online Article Text |
id | pubmed-6830329 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-68303292019-11-20 Blocking LFA-1 Aggravates Cardiac Inflammation in Experimental Autoimmune Myocarditis Weckbach, Ludwig T. Uhl, Andreas Boehm, Felicitas Seitelberger, Valentina Huber, Bruno C. Kania, Gabriela Brunner, Stefan Grabmaier, Ulrich Cells Communication The lymphocyte function-associated antigen 1 (LFA-1) is a member of the beta2-integrin family and plays a pivotal role for T cell activation and leukocyte trafficking under inflammatory conditions. Blocking LFA-1 has reduced or aggravated inflammation depending on the inflammation model. To investigate the effect of LFA-1 in myocarditis, mice with experimental autoimmune myocarditis (EAM) were treated with a function blocking anti-LFA-1 antibody from day 1 of disease until day 21, the peak of inflammation. Cardiac inflammation was evaluated by measuring infiltration of leukocytes into the inflamed cardiac tissue using histology and flow cytometry and was assessed by analysis of the heart weight/body weight ratio. LFA-1 antibody treatment severely enhanced leukocyte infiltration, in particular infiltration of CD11b+ monocytes, F4/80+ macrophages, CD4+ T cells, Ly6G+ neutrophils, and CD133+ progenitor cells at peak of inflammation which was accompanied by an increased heart weight/body weight ratio. Thus, blocking LFA-1 starting at the time of immunization severely aggravated acute cardiac inflammation in the EAM model. MDPI 2019-10-17 /pmc/articles/PMC6830329/ /pubmed/31627327 http://dx.doi.org/10.3390/cells8101267 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Communication Weckbach, Ludwig T. Uhl, Andreas Boehm, Felicitas Seitelberger, Valentina Huber, Bruno C. Kania, Gabriela Brunner, Stefan Grabmaier, Ulrich Blocking LFA-1 Aggravates Cardiac Inflammation in Experimental Autoimmune Myocarditis |
title | Blocking LFA-1 Aggravates Cardiac Inflammation in Experimental Autoimmune Myocarditis |
title_full | Blocking LFA-1 Aggravates Cardiac Inflammation in Experimental Autoimmune Myocarditis |
title_fullStr | Blocking LFA-1 Aggravates Cardiac Inflammation in Experimental Autoimmune Myocarditis |
title_full_unstemmed | Blocking LFA-1 Aggravates Cardiac Inflammation in Experimental Autoimmune Myocarditis |
title_short | Blocking LFA-1 Aggravates Cardiac Inflammation in Experimental Autoimmune Myocarditis |
title_sort | blocking lfa-1 aggravates cardiac inflammation in experimental autoimmune myocarditis |
topic | Communication |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6830329/ https://www.ncbi.nlm.nih.gov/pubmed/31627327 http://dx.doi.org/10.3390/cells8101267 |
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