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From the Department of Pathology, The University of Michigan Medical School, Ann Arbor, Michigan
Matrix metalloproteases (MMPs) are a group of zinc-dependent
endopeptidases that can degrade every component of the extracellular
matrix. Under normal circumstances, the levels of MMPs are
tightly regulated at both transcriptional and posttranscriptional
levels. However, they are up-regulated in pathological states
such as inflammation. Previous investigations have suggested that
MMP-12 (metalloelastase) may be an important mediator in the
pathogenesis of chronic lung injury. In this study we investigated the
role of metalloelastase in the pathogenesis of acute lung injury using
mice containing a targeted disruption of the metalloelastase gene.
Neutrophil influx into the alveolar space in metalloelastase-deficient
animals was reduced to 
50% of that observed in parent strain mice
following the induction of injury by immune complexes. In
addition, lung permeability in metalloelastase-deficient mice
was 50% of that of injured parent strain animals with normal levels
of metalloelastase and this was correlated with histological evidence
of less lung injury in the metalloelastase-deficient animals.
Collectively, the data suggest that metalloelastase is
necessary for the full development of acute alveolitis in this model of
lung injury. Further, the data suggest that reduced injury in
metalloelastase-deficient mice is due in part to decreased neutrophil
influx into the alveolar space.
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