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Hemorrhagic shock primes for increased expression of cytokine-induced neutrophil chemoattractant in the lung: role in pulmonary inflammation following lipopolysaccharide

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dc.contributor.authorFan, Jie
dc.contributor.authorMarshall, John C.
dc.contributor.authorJimenez, María F.
dc.contributor.authorShek, Pang N.
dc.contributor.authorZagorski, John
dc.contributor.authorRotstein, Ori D.
dc.contributor.corporatenamePontificia Universidad Javeriana. Facultad de Medicina. Departamento de Cirugía y Especialidades. Grupo de Investigación de Cirugía y Especialidades
dc.date.accessioned2020-08-25T21:46:40Z
dc.date.available2020-08-25T21:46:40Z
dc.date.created1998
dc.description.abstractenglishRecent studies have suggested that hemorrhagic shock followed by resuscitation renders patients more susceptible to lung injury by priming for an exaggerated response to a second stimulus, the so-called "two-hit" hypothesis. We investigated the role of C-X-C chemokines in mediating the augmented lung inflammation in response to LPS following resuscitated shock. In a rodent model, animals exposed to antecedent shock exhibited enhanced lung neutrophil sequestration and transpulmonary albumin flux in response to intratracheal LPS. This effect correlated with an exaggerated expression of cytokine-induced neutrophil chemoattractant (CINC) protein and mRNA, but not macrophage-inflammatory protein 2. Strategies designed to inhibit CINC, both anti-CINC Ab and supplementation with the antioxidant N-acetyl-cysteine, prevented the enhanced neutrophil sequestration, suggesting that CINC played a central role in the enhanced leukocyte accumulation following shock plus LPS treatment. Shock alone increased lung nuclear factor-kappaB expression and augmented the response to LPS. Prevention of this effect by N-acetylcysteine supplementation of the resuscitation fluid implicates a role for oxidant stress in the priming for lung inflammation following shock. Finally, alveolar macrophages recovered from shock-resuscitated animals released more CINC protein in vitro in response to LPS than macrophages from sham animals. Considered together, these findings show that augmented release of CINC, in part from primed alveolar macrophages, contributes significantly to the enhanced lung leukosequestration and transpulmonary albumin flux in response to LPS following resuscitated shock.spa
dc.description.paginas440-447spa
dc.description.quartilescopusQ1spa
dc.description.quartilewosQ2spa
dc.formatPDFspa
dc.format.mimetypeapplication/pdfspa
dc.format.soportePapel / Electrónicospa
dc.identifierhttps://www.jimmunol.org/content/jimmunol/161/1/440.full.pdfspa
dc.identifier.issn0022-1767 / 1550-6606 (Electrónico)spa
dc.identifier.urihttp://hdl.handle.net/10554/50858
dc.languageInglésspa
dc.rights.licenceAtribución-NoComercial 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc/4.0/*
dc.sourceJournal of Immunology; Vol. 161 Núm. 1 (1998)spa
dc.titleHemorrhagic shock primes for increased expression of cytokine-induced neutrophil chemoattractant in the lung: role in pulmonary inflammation following lipopolysaccharidespa
dc.typeinfo:eu-repo/semantics/article
dc.type.hasversionhttp://purl.org/coar/version/c_ab4af688f83e57aa
dc.type.localArtículo de revistaspa

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