Lung production of platelet-activating factor acetylhydrolase in oleic acid-induced acute lung injury

被引:12
|
作者
Salluh, Jorge I.
Pino, Alexandre V.
Silva, Adriana R.
Gomes, Rachel N.
Souza, Heitor S.
Silva, Jose Roberto Lapa e
Jandre, Frederico C.
Giannella-Neto, Antonio
Zimmerman, Guy A.
Stafforini, Diana M.
Prescott, Stephen M.
Castro-Faria-Neto, Hugo C.
Bozza, Patricia T.
Bozza, Fernando A.
机构
[1] Fundacao Oswaldo Cruz, IOC, Dept Physiol & Pharmacodynam, Immunopharmacol Lab, BR-21045900 Rio De Janeiro, Brazil
[2] Inst Nacl Canc, Intens Care Unit, Rio De Janeiro, Brazil
[3] Univ Fed Rio de Janeiro, COPPE, Dept Biomed Engn, Pulm Engn Lab, BR-21945 Rio De Janeiro, Brazil
[4] Univ Fed Rio de Janeiro, Hosp Univ Clementino Fraga Filho, Multidisciplinary Lab, Rio De Janeiro, Brazil
[5] Univ Utah, Dept Internal Med, Program Human Mol Biol & Genet, Salt Lake City, UT 84112 USA
[6] Univ Utah, Huntsman Canc Inst, Salt Lake City, UT USA
[7] Fundacao Oswaldo Cruz, Inst Pesquisas Clin Evandro Chagas, ICU, BR-21045900 Rio De Janeiro, Brazil
来源
PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS | 2007年 / 77卷 / 01期
关键词
D O I
10.1016/j.plefa.2007.04.001
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Platelet-activating factor (PAF) is a proinflammatory mediator that plays a central role in acute lung injury (ALI). PAF-acetylhydrolases (PAF-AHs) terminate PAF's signals and regulate inflammation. In this study, we describe the kinetics of plasma and bronchoalveolar lavage (BAL) PAF-AH in the early phase of ALI. Six pigs with oleic acid induced ALI and two healthy controls were studied. Plasma and BAL samples were collected every 2h and immunohistochemical analysis of PAF-AH was performed in lung tissues. PAF-AH activity in BAL was increased at the end of the experiment (BAL PAF-AH Time 0 = 0.001 +/- 0.001 nmol/ml/min/g vs Time 6 = 0.031 +/- 0.018 nmol/ml/min/g, p = 0.04) while plasma activity was not altered. We observed increased PAF-AH staining of macrophages and epithelial cells in the lungs of animals with ALI but not in healthy controls. Our data suggest that increases in PAF-AH levels are, in part, a result of alveolar production. PAF-AH may represent a modulatory strategy to counteract the excessive pro-inflammatory effects of PAF and PAF-like lipids in lung inflammation. (c) 2007 Elsevier Ltd. All rights reserved.
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页码:1 / 8
页数:8
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