Endotoxins, asthma, and allergic immune responses

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dc.contributor.author Silva, JR Lapa
dc.contributor.author Silva, MD Possebon da [UNIFESP]
dc.contributor.author Lefort, J.
dc.contributor.author Vargaftig, B. B.
dc.date.accessioned 2018-06-18T12:15:03Z
dc.date.available 2018-06-18T12:15:03Z
dc.date.issued 2000-11-02
dc.identifier http://dx.doi.org/10.1016/S0300-483X(00)00289-4
dc.identifier.citation Toxicology. Clare: Elsevier Ireland Ltd, v. 152, n. 1-3, p. 31-35, 2000.
dc.identifier.issn 0300-483X
dc.identifier.uri http://repositorio.unifesp.br/11600/45666
dc.description.abstract Asthma severity depends to a great extent on the levels of endotoxin present in the microenvironment. Although favouring a Th1 cytokine response that could be beneficial to the asthmatic, lipopolysaccharide (LPS) aggravates bronchopulmonary inflammation by several mechanisms. These include neutrophil and eosinophil recruitment, and release by activated macrophages of pro-inflammatory cytokines and nitric oxide. LPS exerts its biological actions through its interaction with CD14. The genetic locus of CD14 is close to the genomic region controlling levels of IgE. A polymorphism in the CD14 promoter region seems to favour high serum IgE levels. Genetic influences may thus control circulating levels of sCD14 and by this mechanism modulate Th1/Th2 balance and IgE synthesis. LPS exposure, although hazardous to the asthmatic, seems to exert a role in the maturation of the immune system in children towards a Th1-skewed pattern. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved. en
dc.format.extent 31-35
dc.language.iso eng
dc.publisher Elsevier B.V.
dc.relation.ispartof Toxicology
dc.rights Acesso restrito
dc.subject LPS en
dc.subject allergy en
dc.subject CD14 en
dc.subject cytokines en
dc.title Endotoxins, asthma, and allergic immune responses en
dc.type Artigo
dc.rights.license http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.contributor.institution Inst Pasteur
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.contributor.institution Universidade Federal do Rio de Janeiro (UFRJ)
dc.description.affiliation Inst Pasteur, INSERM 485, Unite Pharmacol Cellulaire, F-75724 Paris 15, France
dc.description.affiliation Univ Fed Sao Paulo, Escola Paulista Med, Sao Paulo, Brazil
dc.description.affiliation Univ Fed Rio de Janeiro, Hosp Univ Clementino Fraga Filho, Rio De Janeiro, Brazil
dc.description.affiliationUnifesp Univ Fed Sao Paulo, Escola Paulista Med, Sao Paulo, Brazil
dc.identifier.doi 10.1016/S0300-483X(00)00289-4
dc.description.source Web of Science
dc.identifier.wos WOS:000165627100005


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