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From the Divisions of Pulmonary and Critical Care
Medicine *
and Allergy and Infectious
Diseases
of the Department of
Medicine, the Department of Surgery,
and the
Department of Pathology,§
University of
Washington, Seattle, Washington
Activation of the Fas/FasL system induces apoptosis of susceptible
cells, but may also lead to nuclear factor 
B activation. Our
goal was to determine whether local Fas activation produces acute lung
injury by inducing alveolar epithelial cell apoptosis and by generating
local inflammatory responses. Normal mice (C57BL/6) and mice deficient
in Fas (lpr) were treated by intranasal instillation of
the Fas-activating monoclonal antibody (mAb) Jo2 or an irrelevant
control mAb, and studied 6 or 24 hours later using
bronchoalveolar lavage (BAL), histopathology, DNA
nick-end-labeling assays, and electron microscopy. Normal mice
treated with mAb Jo2 had significant increases in BAL protein at 6
hours, and BAL neutrophils at 24 hours, as compared to
lpr mice and to mice treated with the irrelevant mAb.
Neutrophil recruitment was preceded by increased mRNA expression for
tumor necrosis factor-
, macrophage inflammatory
protein-1, macrophage inflammatory protein-2,
macrophage chemotactic protein-1, and
interleukin-6, but not interferon-
, transforming
growth factor-ß, RANTES, eotaxin,
or IP-10. Lung sections from Jo2-treated normal mice showed
neutrophilic infiltrates, alveolar septal thickening,
hemorrhage, and terminal dUTP nick-end-labeling-positive cells
in the alveolar septae and airspaces. Type II pneumocyte apoptosis was
confirmed by electron microscopy. Fas activation in vivo
results in acute alveolar epithelial injury and lung
inflammation, and may be important in the pathogenesis of acute
lung injury.
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