CD43 sialoglycoprotein modulates cardiac inflammation and murine susceptibility to Trypanosoma cruzi infection

Abstract CD43 (leukosialin) is a large sialoglycoprotein abundantly expressed on the surface of most cells from the hematopoietic lineage. CD43 is directly involved in the contact between cells participating in a series of events such as signaling, adherence and host parasite interactions. In this s...

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Autores principales:	Frederico Alisson-Silva, Natália Rodrigues Mantuano, Ana Luiza Lopes, Andréia Vasconcelos-dos-Santos, André Macedo Vale, Miriam Maria Costa, Judy L. Cannon, Ana Carolina Oliveira, Adriane R. Todeschini
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2019
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/2f985969b6a54c9f94d0f63024d3025a
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spelling	oai:doaj.org-article:2f985969b6a54c9f94d0f63024d3025a2021-12-02T15:08:09ZCD43 sialoglycoprotein modulates cardiac inflammation and murine susceptibility to Trypanosoma cruzi infection10.1038/s41598-019-45138-72045-2322https://doaj.org/article/2f985969b6a54c9f94d0f63024d3025a2019-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-019-45138-7https://doaj.org/toc/2045-2322Abstract CD43 (leukosialin) is a large sialoglycoprotein abundantly expressed on the surface of most cells from the hematopoietic lineage. CD43 is directly involved in the contact between cells participating in a series of events such as signaling, adherence and host parasite interactions. In this study we examined the role of CD43 in the immune response against Trypanosoma cruzi, the protozoan parasite that causes Chagas’ disease, a potential life-threatening illness endemic in 21 Latin American countries according to the WHO. The acute stage of infection is marked by intense parasitemia and cardiac tissue parasitism, resulting in the recruitment of inflammatory cells and acute damage to the heart tissue. We show here that CD43 −/− mice were more resistant to infection due to increased cytotoxicity of antigen specific CD8+ T cells and reduced inflammatory infiltration in the cardiac tissue, both contributing to lower cardiomyocyte damage. In addition, we demonstrate that the induction of acute myocarditis involves the engagement of CD43 cytoplasmic tripeptide sequence KRR to ezrin-radixin-moiesin cytoskeletal proteins. Together, our results show the participation of CD43 in different events involved in the pathogenesis of T. cruzi infection, contributing to a better overall understanding of the mechanisms underlying the pathogenesis of acute chagasic cardiomyopathy.Frederico Alisson-SilvaNatália Rodrigues MantuanoAna Luiza LopesAndréia Vasconcelos-dos-SantosAndré Macedo ValeMiriam Maria CostaJudy L. CannonAna Carolina OliveiraAdriane R. TodeschiniNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 9, Iss 1, Pp 1-11 (2019)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Frederico Alisson-Silva Natália Rodrigues Mantuano Ana Luiza Lopes Andréia Vasconcelos-dos-Santos André Macedo Vale Miriam Maria Costa Judy L. Cannon Ana Carolina Oliveira Adriane R. Todeschini CD43 sialoglycoprotein modulates cardiac inflammation and murine susceptibility to Trypanosoma cruzi infection
description	Abstract CD43 (leukosialin) is a large sialoglycoprotein abundantly expressed on the surface of most cells from the hematopoietic lineage. CD43 is directly involved in the contact between cells participating in a series of events such as signaling, adherence and host parasite interactions. In this study we examined the role of CD43 in the immune response against Trypanosoma cruzi, the protozoan parasite that causes Chagas’ disease, a potential life-threatening illness endemic in 21 Latin American countries according to the WHO. The acute stage of infection is marked by intense parasitemia and cardiac tissue parasitism, resulting in the recruitment of inflammatory cells and acute damage to the heart tissue. We show here that CD43 −/− mice were more resistant to infection due to increased cytotoxicity of antigen specific CD8+ T cells and reduced inflammatory infiltration in the cardiac tissue, both contributing to lower cardiomyocyte damage. In addition, we demonstrate that the induction of acute myocarditis involves the engagement of CD43 cytoplasmic tripeptide sequence KRR to ezrin-radixin-moiesin cytoskeletal proteins. Together, our results show the participation of CD43 in different events involved in the pathogenesis of T. cruzi infection, contributing to a better overall understanding of the mechanisms underlying the pathogenesis of acute chagasic cardiomyopathy.
format	article
author	Frederico Alisson-Silva Natália Rodrigues Mantuano Ana Luiza Lopes Andréia Vasconcelos-dos-Santos André Macedo Vale Miriam Maria Costa Judy L. Cannon Ana Carolina Oliveira Adriane R. Todeschini
author_facet	Frederico Alisson-Silva Natália Rodrigues Mantuano Ana Luiza Lopes Andréia Vasconcelos-dos-Santos André Macedo Vale Miriam Maria Costa Judy L. Cannon Ana Carolina Oliveira Adriane R. Todeschini
author_sort	Frederico Alisson-Silva
title	CD43 sialoglycoprotein modulates cardiac inflammation and murine susceptibility to Trypanosoma cruzi infection
title_short	CD43 sialoglycoprotein modulates cardiac inflammation and murine susceptibility to Trypanosoma cruzi infection
title_full	CD43 sialoglycoprotein modulates cardiac inflammation and murine susceptibility to Trypanosoma cruzi infection
title_fullStr	CD43 sialoglycoprotein modulates cardiac inflammation and murine susceptibility to Trypanosoma cruzi infection
title_full_unstemmed	CD43 sialoglycoprotein modulates cardiac inflammation and murine susceptibility to Trypanosoma cruzi infection
title_sort	cd43 sialoglycoprotein modulates cardiac inflammation and murine susceptibility to trypanosoma cruzi infection
publisher	Nature Portfolio
publishDate	2019
url	https://doaj.org/article/2f985969b6a54c9f94d0f63024d3025a
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CD43 sialoglycoprotein modulates cardiac inflammation and murine susceptibility to Trypanosoma cruzi infection

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