Acute lung injury: Apoptosis and signaling mechanisms

Document Type

Article

Publication Date

2009

Abstract

Acute lung injury (ALI) has been documented clinically following several pathological states such as trauma, septic shock and pneumonia. The histopathological characteristics, paired with the production of a number of cellular pro-inflammatory mediators, play a crucial role in the progression of ALI. During ALI, polymorphonuclear neutrophil (PMN)-mediated apoptosis is delayed by macrophages, possibly via effects on the Fas/FasL mediated pathway, leading to the accumulation of these cells at the site of injury and inflammation. The transcriptional regulation of NFkB, CREB, and AP-1 also regulates the pathogenesis of ALI. During sepsis and septic shock, we found evidence of infiltrating leukocytes in the alveolar spaces along with an increased number of TUNEL-positive cells in the lung sections. We also observed an increased expression of TRADD and Bax/Bcl2 ratio at 7 days post-sepsis. In contrast, the NFkB/IkB ratio increased at 1 day post-sepsis. Together, these data provide evidence illustrating the induction of apoptosis in lung tissues subsequent to the onset of polymicrobial sepsis. The results support the concept that the upregulation of apoptosis following lung inflammation plays a crucial role in the development of acute lung injury and related disorders such as ARDS.

Publication Title

Experimental biology and medicine

Volume

234

Issue

4

First Page

361

Last Page

371

Comments

This article was published in Experimental biology and medicine, Volume 234, Issue 4, Pages 361-371.

The published version is available at http://dx.doi.org/10.3181/0811-MR-318.

Copyright © 2009 SEBM.

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