• Mônica C M Chao, Cristiane S N B Garcia, Mariana B G de Oliveira, Raquel S Santos, Isabela H Lucas, Pedro L Silva, Adriana Vieira-Abreu, Hugo C de Castro-Faria-Neto, Edwin R Parra-Cuentas, Vera L Capelozzi, Paolo Pelosi, and Patricia R M Rocco.
• Laboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
• Respir Physiol Neurobiol. 2010 Sep 30;173(2):179-88.

AbstractWe tested the hypothesis that at the early phase of acute lung injury (ALI) the degree of endothelium injury may predict lung parenchyma remodelling. For this purpose, two models of extrapulmonary ALI induced by Escherichia coli lipopolysaccharide (ALI-LPS) or cecal ligation and puncture (ALI-CLP) were developed in mice. At day 1, these models had similar degrees of lung mechanical compromise, epithelial damage, and intraperitoneal inflammation, but endothelial lesion was greater in ALI-CLP. A time course analysis revealed, at day 7: ALI-CLP had higher degrees of epithelial lesion, denudation of basement membrane, endothelial damage, elastic and collagen fibre content, neutrophils in bronchoalveolar lavage fluid (BALF), peritoneal fluid and blood, levels of interleukin-6, KC (murine analogue of IL-8), and transforming growth factor-β in BALF. Conversely, the number of lung apoptotic cells was similar in both groups. In conclusion, the intensity of fibroelastogenesis was affected by endothelium injury in addition to the maintenance of epithelial damage and intraperitoneal inflammation.Copyright 2010 Elsevier B.V. All rights reserved.

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