Fas-induced pulmonary apoptosis and inflammation during indirect acute lung injury.

ABSTRACT:

Rationale

Indirect acute lung injury (ALI) is associated with high morbidity and mortality. No specific therapies have been developed, because the underlying pathophysiological processes remain elusive.

Objectives

To investigate the contribution of Fas-induced apoptotic and nonapoptotic/inflammatory signaling to the pathology of indirect ALI.

Methods

A mouse model of indirect ALI, induced by successive exposure to hemorrhagic shock and cecal ligation and puncture, was used. Quantification of active caspase-3 and the short splice variant of FLICE-inhibitory protein, (FLIP)short, was performed by Western blotting and immunohistochemistry, and cytokines/chemokines were assessed by cytometric bead array or ELISA. M30 immunostaining was done to evaluate epithelial cell apo

SUBMITTER: Perl M 

PROVIDER: S-EPMC1994224 | biostudies-literature | 2007 Sep

REPOSITORIES: biostudies-literature