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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Public Library of Science (PLoS)
2012
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oai:doaj.org-article:0483c2a07a744bf69a5dacd09fceecaf2021-11-18T07:17:32ZTLR2, TLR4 and the MYD88 signaling pathway are crucial for neutrophil migration in acute kidney injury induced by sepsis.1932-620310.1371/journal.pone.0037584https://doaj.org/article/0483c2a07a744bf69a5dacd09fceecaf2012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22655058/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203The 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.Angela CastoldiTárcio Teodoro BragaMatheus Correa-CostaCristhiane Fávero AguiarÊnio José BassiReinaldo Correa-SilvaRosa Maria EliasFábia SalvadorPedro Manoel Moraes-VieiraMarcos Antônio CenedezeMarlene Antônia ReisMeire Ioshie HiyaneÁlvaro Pacheco-SilvaGiselle Martins GonçalvesNiels Olsen Saraiva CâmaraPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 5, p e37584 (2012) |
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Medicine R Science Q Angela Castoldi Tárcio Teodoro Braga Matheus Correa-Costa Cristhiane Fávero Aguiar Ênio José Bassi Reinaldo Correa-Silva Rosa Maria Elias Fábia Salvador Pedro Manoel Moraes-Vieira Marcos Antônio Cenedeze Marlene Antônia Reis Meire Ioshie Hiyane Álvaro Pacheco-Silva Giselle Martins Gonçalves Niels Olsen Saraiva Câmara TLR2, TLR4 and the MYD88 signaling pathway are crucial for neutrophil migration in acute kidney injury induced by sepsis. |
| 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. |
| format |
article |
| author |
Angela Castoldi Tárcio Teodoro Braga Matheus Correa-Costa Cristhiane Fávero Aguiar Ênio José Bassi Reinaldo Correa-Silva Rosa Maria Elias Fábia Salvador Pedro Manoel Moraes-Vieira Marcos Antônio Cenedeze Marlene Antônia Reis Meire Ioshie Hiyane Álvaro Pacheco-Silva Giselle Martins Gonçalves Niels Olsen Saraiva Câmara |
| author_facet |
Angela Castoldi Tárcio Teodoro Braga Matheus Correa-Costa Cristhiane Fávero Aguiar Ênio José Bassi Reinaldo Correa-Silva Rosa Maria Elias Fábia Salvador Pedro Manoel Moraes-Vieira Marcos Antônio Cenedeze Marlene Antônia Reis Meire Ioshie Hiyane Álvaro Pacheco-Silva Giselle Martins Gonçalves Niels Olsen Saraiva Câmara |
| author_sort |
Angela Castoldi |
| title |
TLR2, TLR4 and the MYD88 signaling pathway are crucial for neutrophil migration in acute kidney injury induced by sepsis. |
| 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. |
| publisher |
Public Library of Science (PLoS) |
| publishDate |
2012 |
| url |
https://doaj.org/article/0483c2a07a744bf69a5dacd09fceecaf |
| work_keys_str_mv |
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