Bradykinin inducible receptor is essential to lipopolysaccharide-induced acute lung injury in mice

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dc.contributor.author Campanholle, Gabriela
dc.contributor.author Landgraf, Richardt G. [UNIFESP]
dc.contributor.author Borducchi, Erica
dc.contributor.author Semedo, Patricia [UNIFESP]
dc.contributor.author Wang, Pamela H. M. [UNIFESP]
dc.contributor.author Amano, Mariane T.
dc.contributor.author Russo, Momtchilo
dc.contributor.author Pacheco-Silva, Alvaro [UNIFESP]
dc.contributor.author Jancar, Sonia
dc.contributor.author Camara, Niels O. S. [UNIFESP]
dc.date.accessioned 2016-01-24T13:59:42Z
dc.date.available 2016-01-24T13:59:42Z
dc.date.issued 2010-05-25
dc.identifier http://dx.doi.org/10.1016/j.ejphar.2010.02.002
dc.identifier.citation European Journal of Pharmacology. Amsterdam: Elsevier B.V., v. 634, n. 1-3, p. 132-137, 2010.
dc.identifier.issn 0014-2999
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/32550
dc.description.abstract Lipopolysaccharides from gram-negative bacteria are amongst the most common causative agents of acute lung injury, which is characterized by an inflammatory response, with cellular infiltration and the release of mediators/cytokines. There is evidence that bradykinin plays a role in lung inflammation in asthma but in other types of lung inflammation its role is less clear. in the present study we evaluated the role of the bradykinin B(1) receptor in acute lung injury caused by lipopolysaccharide inhalation and the mechanisms behind bradykinin actions participating in the inflammatory response. We found that in C57BI/6 mice, the bradykinin B(1) receptor expression was up-regulated 24 h after lipopolysaccharide inhalation. At this time, the number of cells and protein concentration were significantly increased in the bronchoalveolar lavage fluid and the mice developed airway hyperreactivity to methacholine. in addition, there was an increased expression of tumor necrosis factor-alpha, interleukin-1 beta and interferon-gamma and chemokines (monocytes chemotactic protein-1 and KC) in the bronchoalveolar lavage fluid and in the lung tissue. We then treated the mice with a bradykinin B, receptor antagonist, R-954 (Ac-Orn-[Oic(2), alpha-MePhe(5), D-beta Nal(7), Ile(8)]desArg(9)-bradykinin), 30 min after lipopolysaccharide administration. We observed that this treatment prevented the airway hyperreactivity as well as the increased cellular infiltration and protein content in the bronchoalveolar lavage fluid. Moreover, R-954 inhibited the expression of cytokines/chemokines. These results implicate bradykinin, acting through B(1) receptor, in the development of acute lung injury caused by lipopolysaccharide inhalation. (C) 2010 Elsevier B.V. All rights reserved. en
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorship INCT Complex Fluids
dc.description.sponsorship Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.format.extent 132-137
dc.language.iso eng
dc.publisher Elsevier B.V.
dc.relation.ispartof European Journal of Pharmacology
dc.rights Acesso restrito
dc.subject Lipopolysaccharide en
dc.subject Bradykinin en
dc.subject Bradykinin B(1) receptor en
dc.subject Acute lung injury en
dc.title Bradykinin inducible receptor is essential to lipopolysaccharide-induced acute lung injury in mice en
dc.type Artigo
dc.rights.license http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.contributor.institution Universidade de São Paulo (USP)
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Univ São Paulo, Lab Transplantat Immunobiol, Dept Immunol, BR-05508900 São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Dept Ciencias Biol, São Paulo, Brazil
dc.description.affiliation Univ São Paulo, Dept Immunol, São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Clin & Expt Immunol Lab, Div Nephrol, São Paulo, Brazil
dc.description.affiliation Univ São Paulo, Lab Immunopharmacol, Dept Immunol, São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Ciencias Biol, São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Clin & Expt Immunol Lab, Div Nephrol, São Paulo, Brazil
dc.description.sponsorshipID FAPESP: 06/06236-2
dc.description.sponsorshipID FAPESP: 06/03982-5
dc.description.sponsorshipID FAPESP: 07/07139-3
dc.identifier.doi 10.1016/j.ejphar.2010.02.002
dc.description.source Web of Science
dc.identifier.wos WOS:000277554900019



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