Relationship of Acute Lung Inflammatory Injury to Fas/FasL System

Overview

Journal Am J Pathol

Publisher Elsevier

Specialty Pathology

Date 2005 Mar 4

PMID 15743781

Citations 36

Authors

Thomas A Neff

Ren-Feng Guo

Simona B Neff

J Vidya Sarma

Cecilia L Speyer

Hongwei Gao

Kurt D Bernacki

Markus Huber-Lang

Stephanie McGuire

L Marco Hoesel

Niels C Riedemann

Beatrice Beck-Schimmer

Firas S Zetoune

Peter A Ward

Affiliations

Soon will be listed here.

Abstract

There is mounting evidence that apoptosis plays a significant role in tissue damage during acute lung injury. To evaluate the role of the apoptosis mediators Fas and FasL in acute lung injury, Fas (lpr)- or FasL (gld)-deficient and wild-type mice were challenged with intrapulmonary deposition of IgG immune complexes. Lung injury parameters ((125)I-albumin leak, accumulation of myeloperoxidase, and wet lung weights) were measured and found to be consistently reduced in both lpr and gld mice. In wild-type mice, lung injury was associated with a marked increase in Fas protein in lung. Inflamed lungs of wild-type mice showed striking evidence of activated caspase-3, which was much diminished in inflamed lungs from lpr mice. Intratracheal administration of a monoclonal Fas-activating antibody (Jo2) in wild-type mice induced MIP-2 and KC production in bronchoalveolar lavage fluids, and a murine alveolar macrophage cell line (MH-S) showed significantly increased MIP-2 production after incubation with this antibody. Bronchoalveolar lavage fluid content of MIP-2 and KC was substantially reduced in lpr mice after lung injury when compared to levels in wild-type mice. These data suggest that the Fas/FasL system regulates the acute lung inflammatory response by positively affecting CXC-chemokine production, ultimately leading to enhanced neutrophil influx and tissue damage.

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