Is serum amyloid A an endogenous TLR4 agonist?
Autor(a) principal: | |
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Data de Publicação: | 2008 |
Outros Autores: | , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://dx.doi.org/10.1189/jlb.0407203 http://repositorio.unifesp.br/handle/11600/30621 |
Resumo: | Serum amyloid A (SAA), a classical acute-phase protein, is produced predominantly by hepatocytes in response to injury, infection, and inflammation. It has been shown that SAA primes leukocytes and induces the expression and release of proinflammatory cytokines. Here, we report that SAA induces NO production by murine peritoneal macrophages. Using specific inhibitors, we showed that NO production was dependent on inducible NO synthase thorough the activation of ERK1/2 and p38 MAPKs. Moreover, SAA activity was decreased after proteolysis but not with polymyxin B, a lipid A antagonist. Finally, we found that NO production was dependent on functional TLR4, a receptor complex associated with innate immunity. Macrophages from C3H/HeJ and C57BL/10ScCr mice lacking a functional TLR4 did not respond to SAA stimulation. in conclusion, our study makes a novel observation that SAA might be an endogenous agonist for the TLR4 complex on macrophages. the contribution of this finding in amplifying innate immunity during the inflammatory process is discussed. |
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Repositório Institucional da UNIFESP |
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Is serum amyloid A an endogenous TLR4 agonist?toll like receptorsmacrophagesnitric oxide (NO)Serum amyloid A (SAA), a classical acute-phase protein, is produced predominantly by hepatocytes in response to injury, infection, and inflammation. It has been shown that SAA primes leukocytes and induces the expression and release of proinflammatory cytokines. Here, we report that SAA induces NO production by murine peritoneal macrophages. Using specific inhibitors, we showed that NO production was dependent on inducible NO synthase thorough the activation of ERK1/2 and p38 MAPKs. Moreover, SAA activity was decreased after proteolysis but not with polymyxin B, a lipid A antagonist. Finally, we found that NO production was dependent on functional TLR4, a receptor complex associated with innate immunity. Macrophages from C3H/HeJ and C57BL/10ScCr mice lacking a functional TLR4 did not respond to SAA stimulation. in conclusion, our study makes a novel observation that SAA might be an endogenous agonist for the TLR4 complex on macrophages. the contribution of this finding in amplifying innate immunity during the inflammatory process is discussed.Univ São Paulo, Inst Biomed Sci, Dept Immunol, BR-05508000 São Paulo, BrazilUniv São Paulo, Dept Clin Anal & Toxicol, Fac Pharmaceut Sci, BR-05508000 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biochem Mol Biol, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biochem Mol Biol, São Paulo, BrazilWeb of ScienceFederation Amer Soc Exp BiolUniversidade de São Paulo (USP)Universidade Federal de São Paulo (UNIFESP)Sandri, SilvanaRodriguez, DuniaGomes, ElianeMonteiro, Hugo Pequeno [UNIFESP]Russo, MomtchiloCampa, Ana2016-01-24T13:49:46Z2016-01-24T13:49:46Z2008-05-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion1174-1180http://dx.doi.org/10.1189/jlb.0407203Journal of Leukocyte Biology. Bethesda: Federation Amer Soc Exp Biol, v. 83, n. 5, p. 1174-1180, 2008.10.1189/jlb.04072030741-5400http://repositorio.unifesp.br/handle/11600/30621WOS:000258019500012engJournal of Leukocyte Biologyinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2024-10-14T13:51:15Zoai:repositorio.unifesp.br/:11600/30621Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652024-10-14T13:51:15Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.none.fl_str_mv |
Is serum amyloid A an endogenous TLR4 agonist? |
title |
Is serum amyloid A an endogenous TLR4 agonist? |
spellingShingle |
Is serum amyloid A an endogenous TLR4 agonist? Sandri, Silvana toll like receptors macrophages nitric oxide (NO) |
title_short |
Is serum amyloid A an endogenous TLR4 agonist? |
title_full |
Is serum amyloid A an endogenous TLR4 agonist? |
title_fullStr |
Is serum amyloid A an endogenous TLR4 agonist? |
title_full_unstemmed |
Is serum amyloid A an endogenous TLR4 agonist? |
title_sort |
Is serum amyloid A an endogenous TLR4 agonist? |
author |
Sandri, Silvana |
author_facet |
Sandri, Silvana Rodriguez, Dunia Gomes, Eliane Monteiro, Hugo Pequeno [UNIFESP] Russo, Momtchilo Campa, Ana |
author_role |
author |
author2 |
Rodriguez, Dunia Gomes, Eliane Monteiro, Hugo Pequeno [UNIFESP] Russo, Momtchilo Campa, Ana |
author2_role |
author author author author author |
dc.contributor.none.fl_str_mv |
Universidade de São Paulo (USP) Universidade Federal de São Paulo (UNIFESP) |
dc.contributor.author.fl_str_mv |
Sandri, Silvana Rodriguez, Dunia Gomes, Eliane Monteiro, Hugo Pequeno [UNIFESP] Russo, Momtchilo Campa, Ana |
dc.subject.por.fl_str_mv |
toll like receptors macrophages nitric oxide (NO) |
topic |
toll like receptors macrophages nitric oxide (NO) |
description |
Serum amyloid A (SAA), a classical acute-phase protein, is produced predominantly by hepatocytes in response to injury, infection, and inflammation. It has been shown that SAA primes leukocytes and induces the expression and release of proinflammatory cytokines. Here, we report that SAA induces NO production by murine peritoneal macrophages. Using specific inhibitors, we showed that NO production was dependent on inducible NO synthase thorough the activation of ERK1/2 and p38 MAPKs. Moreover, SAA activity was decreased after proteolysis but not with polymyxin B, a lipid A antagonist. Finally, we found that NO production was dependent on functional TLR4, a receptor complex associated with innate immunity. Macrophages from C3H/HeJ and C57BL/10ScCr mice lacking a functional TLR4 did not respond to SAA stimulation. in conclusion, our study makes a novel observation that SAA might be an endogenous agonist for the TLR4 complex on macrophages. the contribution of this finding in amplifying innate immunity during the inflammatory process is discussed. |
publishDate |
2008 |
dc.date.none.fl_str_mv |
2008-05-01 2016-01-24T13:49:46Z 2016-01-24T13:49:46Z |
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/10.1189/jlb.0407203 Journal of Leukocyte Biology. Bethesda: Federation Amer Soc Exp Biol, v. 83, n. 5, p. 1174-1180, 2008. 10.1189/jlb.0407203 0741-5400 http://repositorio.unifesp.br/handle/11600/30621 WOS:000258019500012 |
url |
http://dx.doi.org/10.1189/jlb.0407203 http://repositorio.unifesp.br/handle/11600/30621 |
identifier_str_mv |
Journal of Leukocyte Biology. Bethesda: Federation Amer Soc Exp Biol, v. 83, n. 5, p. 1174-1180, 2008. 10.1189/jlb.0407203 0741-5400 WOS:000258019500012 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Journal of Leukocyte Biology |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
1174-1180 |
dc.publisher.none.fl_str_mv |
Federation Amer Soc Exp Biol |
publisher.none.fl_str_mv |
Federation Amer Soc Exp Biol |
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 |
_version_ |
1814268454821167104 |