TLR2, TLR4 and the MYD88 Signaling Pathway Are Crucial for Neutrophil Migration in Acute Kidney Injury Induced by Sepsis

Castoldi, Angela [UNIFESP]; Braga, Tarcio Teodoro; Correa-Costa, Matheus; Aguiar, Cristhiane Fávero [UNIFESP]; Bassi, Enio Jose; Correa-Silva, Reinaldo [UNIFESP]; Elias, Rosa Maria [UNIFESP]; Salvador, Fabia [UNIFESP]; Moraes-Vieira, Pedro Manoel; Cenedeze, Marcos Antonio [UNIFESP]; Reis, Marlene Antonia; Hiyane, Meire Ioshie; Pacheco-Silva, Alvaro [UNIFESP]; Goncalves, Giselle Martins; Câmara, Niels Olsen Saraiva [UNIFESP]

TLR2, TLR4 and the MYD88 Signaling Pathway Are Crucial for Neutrophil Migration in Acute Kidney Injury Induced by Sepsis

The aim of this study was to investigate the role of TLR2, TLR4 and MyD88 in sepsis-induced AKI. C57BL/6 TLR2(-/-), TLR4(-/-) and MyD88(-/-) male mice were subjected to sepsis by cecal ligation and puncture (CLP). Twenty four hours later, kidney tissue and blood samples were collected for analysis....

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Authors:	Castoldi, Angela [UNIFESP], Braga, Tarcio Teodoro, Correa-Costa, Matheus, Aguiar, Cristhiane Fávero [UNIFESP], Bassi, Enio Jose, Correa-Silva, Reinaldo [UNIFESP], Elias, Rosa Maria [UNIFESP], Salvador, Fabia [UNIFESP], Moraes-Vieira, Pedro Manoel, Cenedeze, Marcos Antonio [UNIFESP], Reis, Marlene Antonia, Hiyane, Meire Ioshie, Pacheco-Silva, Alvaro [UNIFESP], Goncalves, Giselle Martins, Câmara, Niels Olsen Saraiva [UNIFESP]
Format:	article
Status:	Published version
Publication Date:	2012
Country:	Brasil
Institution:	Universidade Federal de São Paulo (UNIFESP)
Repository:	Repositório Institucional da UNIFESP
Language:	English
OAI Identifier:	oai:repositorio.unifesp.br:11600/34901
Online Access:	http://dx.doi.org/10.1371/journal.pone.0037584 http://repositorio.unifesp.br/handle/11600/34901
Access Level:	Open access

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spelling	TLR2, TLR4 and the MYD88 Signaling Pathway Are Crucial for Neutrophil Migration in Acute Kidney Injury Induced by SepsisThe aim of this study was to investigate the role of TLR2, TLR4 and MyD88 in sepsis-induced AKI. C57BL/6 TLR2(-/-), TLR4(-/-) and MyD88(-/-) male mice were subjected to sepsis by cecal ligation and puncture (CLP). Twenty four hours later, kidney tissue and blood samples were collected for analysis. the TLR2(-/-), TLR4(-/-) and MyD88(-/-) mice that were subjected to CLP had preserved renal morphology, and fewer areas of hypoxia and apoptosis compared with the wild-type C57BL/6 mice (WT). MyD88(-/-) mice were completely protected compared with the WT mice. We also observed reduced expression of proinflammatory cytokines in the kidneys of the knockout mice compared with those of the WT mice and subsequent inhibition of increased vascular permeability in the kidneys of the knockout mice. the WT mice had increased GR1(+low) cells migration compared with the knockout mice and decreased in GR1(+high) cells migration into the peritoneal cavity. the TLR2(-/-), TLR4(-/-), and MyD88(-/-) mice had lower neutrophil infiltration in the kidneys. Depletion of neutrophils in the WT mice led to protection of renal function and less inflammation in the kidneys of these mice. Innate immunity participates in polymicrobial sepsis-induced AKI, mainly through the MyD88 pathway, by leading to an increased migration of neutrophils to the kidney, increased production of proinflammatory cytokines, vascular permeability, hypoxia and apoptosis of tubular cells.Universidade Federal de São Paulo, Dept Med, Disciplina Nefrol, São Paulo, BrazilUniv São Paulo, Dept Imunol, Lab Imunobiol Transplantes, São Paulo, BrazilHosp Israelita Albert Einstein, IIEP, São Paulo, BrazilUniv Fed Triangulo Mineiro, Uberaba, BrazilUniversidade Federal de São Paulo, Dept Med, Disciplina Nefrol, São Paulo, BrazilWeb of ScienceFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)National Institute of Science and Technology (INCT)FAPESP: 07/07139-3Public Library ScienceUniversidade Federal de São Paulo (UNIFESP)Universidade de São Paulo (USP)Hosp Israelita Albert EinsteinUniv Fed Triangulo Mineiro2016-01-24T14:27:15Z2016-01-24T14:27:15Z2012-05-24info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion14application/pdfhttp://dx.doi.org/10.1371/journal.pone.0037584Plos One. San Francisco: Public Library Science, v. 7, n. 5, 14 p., 2012.10.1371/journal.pone.0037584WOS000305338900034.pdf1932-6203http://repositorio.unifesp.br/handle/11600/34901WOS:000305338900034ark:/48912/001300002dp5xengPlos Oneinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESPCastoldi, Angela [UNIFESP]Braga, Tarcio TeodoroCorrea-Costa, MatheusAguiar, Cristhiane Fávero [UNIFESP]Bassi, Enio JoseCorrea-Silva, Reinaldo [UNIFESP]Elias, Rosa Maria [UNIFESP]Salvador, Fabia [UNIFESP]Moraes-Vieira, Pedro ManoelCenedeze, Marcos Antonio [UNIFESP]Reis, Marlene AntoniaHiyane, Meire IoshiePacheco-Silva, Alvaro [UNIFESP]Goncalves, Giselle MartinsCâmara, Niels Olsen Saraiva [UNIFESP]2024-08-01T01:13:05Zoai:repositorio.unifesp.br:11600/34901Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652024-08-01T01:13:05Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.none.fl_str_mv	TLR2, TLR4 and the MYD88 Signaling Pathway Are Crucial for Neutrophil Migration in Acute Kidney Injury Induced by Sepsis
title	TLR2, TLR4 and the MYD88 Signaling Pathway Are Crucial for Neutrophil Migration in Acute Kidney Injury Induced by Sepsis
spellingShingle	TLR2, TLR4 and the MYD88 Signaling Pathway Are Crucial for Neutrophil Migration in Acute Kidney Injury Induced by Sepsis Castoldi, Angela [UNIFESP]
title_short	TLR2, TLR4 and the MYD88 Signaling Pathway Are Crucial for Neutrophil Migration in Acute Kidney Injury Induced by Sepsis
title_full	TLR2, TLR4 and the MYD88 Signaling Pathway Are Crucial for Neutrophil Migration in Acute Kidney Injury Induced by Sepsis
title_fullStr	TLR2, TLR4 and the MYD88 Signaling Pathway Are Crucial for Neutrophil Migration in Acute Kidney Injury Induced by Sepsis
title_full_unstemmed	TLR2, TLR4 and the MYD88 Signaling Pathway Are Crucial for Neutrophil Migration in Acute Kidney Injury Induced by Sepsis
title_sort	TLR2, TLR4 and the MYD88 Signaling Pathway Are Crucial for Neutrophil Migration in Acute Kidney Injury Induced by Sepsis
dc.creator.none.fl_str_mv	Castoldi, Angela [UNIFESP] Braga, Tarcio Teodoro Correa-Costa, Matheus Aguiar, Cristhiane Fávero [UNIFESP] Bassi, Enio Jose Correa-Silva, Reinaldo [UNIFESP] Elias, Rosa Maria [UNIFESP] Salvador, Fabia [UNIFESP] Moraes-Vieira, Pedro Manoel Cenedeze, Marcos Antonio [UNIFESP] Reis, Marlene Antonia Hiyane, Meire Ioshie Pacheco-Silva, Alvaro [UNIFESP] Goncalves, Giselle Martins Câmara, Niels Olsen Saraiva [UNIFESP]
author	Castoldi, Angela [UNIFESP]
author_facet	Castoldi, Angela [UNIFESP] Braga, Tarcio Teodoro Correa-Costa, Matheus Aguiar, Cristhiane Fávero [UNIFESP] Bassi, Enio Jose Correa-Silva, Reinaldo [UNIFESP] Elias, Rosa Maria [UNIFESP] Salvador, Fabia [UNIFESP] Moraes-Vieira, Pedro Manoel Cenedeze, Marcos Antonio [UNIFESP] Reis, Marlene Antonia Hiyane, Meire Ioshie Pacheco-Silva, Alvaro [UNIFESP] Goncalves, Giselle Martins Câmara, Niels Olsen Saraiva [UNIFESP]
author_role	author
author2	Braga, Tarcio Teodoro Correa-Costa, Matheus Aguiar, Cristhiane Fávero [UNIFESP] Bassi, Enio Jose Correa-Silva, Reinaldo [UNIFESP] Elias, Rosa Maria [UNIFESP] Salvador, Fabia [UNIFESP] Moraes-Vieira, Pedro Manoel Cenedeze, Marcos Antonio [UNIFESP] Reis, Marlene Antonia Hiyane, Meire Ioshie Pacheco-Silva, Alvaro [UNIFESP] Goncalves, Giselle Martins Câmara, Niels Olsen Saraiva [UNIFESP]
author2_role	author author author author author author author author author author author author author author
dc.contributor.none.fl_str_mv	Universidade Federal de São Paulo (UNIFESP) Universidade de São Paulo (USP) Hosp Israelita Albert Einstein Univ Fed Triangulo Mineiro
description	The aim of this study was to investigate the role of TLR2, TLR4 and MyD88 in sepsis-induced AKI. C57BL/6 TLR2(-/-), TLR4(-/-) and MyD88(-/-) male mice were subjected to sepsis by cecal ligation and puncture (CLP). Twenty four hours later, kidney tissue and blood samples were collected for analysis. the TLR2(-/-), TLR4(-/-) and MyD88(-/-) mice that were subjected to CLP had preserved renal morphology, and fewer areas of hypoxia and apoptosis compared with the wild-type C57BL/6 mice (WT). MyD88(-/-) mice were completely protected compared with the WT mice. We also observed reduced expression of proinflammatory cytokines in the kidneys of the knockout mice compared with those of the WT mice and subsequent inhibition of increased vascular permeability in the kidneys of the knockout mice. the WT mice had increased GR1(+low) cells migration compared with the knockout mice and decreased in GR1(+high) cells migration into the peritoneal cavity. the TLR2(-/-), TLR4(-/-), and MyD88(-/-) mice had lower neutrophil infiltration in the kidneys. Depletion of neutrophils in the WT mice led to protection of renal function and less inflammation in the kidneys of these mice. Innate immunity participates in polymicrobial sepsis-induced AKI, mainly through the MyD88 pathway, by leading to an increased migration of neutrophils to the kidney, increased production of proinflammatory cytokines, vascular permeability, hypoxia and apoptosis of tubular cells.
publishDate	2012
dc.date.none.fl_str_mv	2012-05-24 2016-01-24T14:27:15Z 2016-01-24T14:27:15Z
dc.type.driver.fl_str_mv	info:eu-repo/semantics/article
dc.type.status.fl_str_mv	info:eu-repo/semantics/publishedVersion
format	article
status_str	publishedVersion
dc.identifier.uri.fl_str_mv	http://dx.doi.org/10.1371/journal.pone.0037584 Plos One. San Francisco: Public Library Science, v. 7, n. 5, 14 p., 2012. 10.1371/journal.pone.0037584 WOS000305338900034.pdf 1932-6203 http://repositorio.unifesp.br/handle/11600/34901 WOS:000305338900034
dc.identifier.dark.fl_str_mv	ark:/48912/001300002dp5x
url	http://dx.doi.org/10.1371/journal.pone.0037584 http://repositorio.unifesp.br/handle/11600/34901
identifier_str_mv	Plos One. San Francisco: Public Library Science, v. 7, n. 5, 14 p., 2012. 10.1371/journal.pone.0037584 WOS000305338900034.pdf 1932-6203 WOS:000305338900034 ark:/48912/001300002dp5x
dc.language.iso.fl_str_mv	eng
language	eng
dc.relation.none.fl_str_mv	Plos One
dc.rights.driver.fl_str_mv	info:eu-repo/semantics/openAccess
eu_rights_str_mv	openAccess
dc.format.none.fl_str_mv	14 application/pdf
dc.publisher.none.fl_str_mv	Public Library Science
publisher.none.fl_str_mv	Public Library Science
dc.source.none.fl_str_mv	reponame:Repositório Institucional da UNIFESP instname:Universidade Federal de São Paulo (UNIFESP) instacron:UNIFESP
instname_str	Universidade Federal de São Paulo (UNIFESP)
instacron_str	UNIFESP
institution	UNIFESP
reponame_str	Repositório Institucional da UNIFESP
collection	Repositório Institucional da UNIFESP
repository.name.fl_str_mv	Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)
repository.mail.fl_str_mv	biblioteca.csp@unifesp.br
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score	15.301603

TLR2, TLR4 and the MYD88 Signaling Pathway Are Crucial for Neutrophil Migration in Acute Kidney Injury Induced by Sepsis

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