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B and inflammation
1 Division of Cell Biology, Department of Physiology, College of Medicine, Ewha Medical Research Center, and Center for Cell Signaling Research, Ewha Women's University, Seoul 158-056; 3 Asan Life Science Institute, and 2 Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul 138-736, Korea
The effect of inhaled nitric oxide
(NO) on inflammatory process in acute lung injury (ALI) is unclear. The
aims of this study were to 1) examine whether inhaled NO
affects the biochemical lung injury parameters and cellular
inflammatory responses and 2) determine the effect of
inhaled NO on the activation of nuclear factor-
B (NF-B) in
lipopolysaccharide (LPS)-induced ALI. Compared with saline controls,
rabbits treated intravenously with LPS showed increases in total
protein and lactate dehydrogenase in the bronchoalveolar lavage (BAL)
fluid, indicating ALI. LPS-treated animals with NO inhalation (LPS-NO)
showed significant decreases in these parameters. Neutrophil numbers in
the BAL fluid, the activity of reactive oxygen species in BAL cells,
and the levels of interleukin (IL)-1
and IL-8 in alveolar
macrophages were increased in LPS-treated animals. In contrast,
neutrophil numbers and these cellular activities were substantially
decreased in LPS-NO animals, compared with LPS-treated animals.
NF-B activation in alveolar macrophages from LPS-treated animals was
also markedly increased, whereas this activity was effectively blocked
in LPS-NO animals. These results suggest that inhaled NO attenuates
LPS-induced ALI and pulmonary inflammation. This attenuation may be
associated with the inhibition of NF-B activation.
lipopolysaccharide; cytokines; oxidants
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