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B in Endotoxemia-Induced Alterations of Lung Neutrophil Apoptosis1
*
Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, Denver, CO 80220; and
Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, NJ 08543
Acute lung injury is frequently associated with endotoxemia
and is characterized by the accumulation in the lungs of large numbers
of neutrophils activated to produce proinflammatory mediators. In the
setting of acute lung injury, the percentage of apoptotic cells among
lung neutrophils is decreased. The transcriptional regulatory factor
NF-
B is activated in neutrophils and other pulmonary cell
populations after endotoxemia and appears to play a central role in the
development of the acute inflammatory process that leads to lung
injury. Because NF-B can modulate apoptosis through increasing
expression of anti-apoptotic proteins, activation of NF-B may
contribute to the alterations in lung neutrophil apoptosis associated
with acute lung injury. In the present experiments, endotoxemia
resulted in decreased apoptosis and increased expression of
anti-apoptotic mediators among lung neutrophils. Amounts of A1,
A20, and Bcl-xL, anti-apoptotic proteins whose
transcription is dependent on NF-B, were increased in lung
neutrophils after endotoxemia. Inhibition of nuclear translocation of
NF-B increased the percentage of apoptotic lung neutrophils after
endotoxemia, but not back to the levels found in unmanipulated animals.
Although inhibition of nuclear translocation of NF-B prevented
endotoxemia-induced increases in Bcl-xL, A1, and A20 in
lung neutrophils, this intervention did not prevent
endotoxemia-associated elevation of Mcl-1, an anti-apoptotic
protein primarily under the transcriptional regulation of CREB. These
results demonstrate that mechanisms independent of NF-B activation
play an important role in modulating lung neutrophil apoptosis after
endotoxemia,
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