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B, and Cyclic AMP Response Element Binding Protein1
Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, Denver, CO 80262
Acute inflammatory lung injury occurs frequently in the setting of
severe infection or blood loss. Accumulation of activated neutrophils
in the lungs and increased pulmonary proinflammatory cytokine levels
are major characteristics of acute lung injury. In the present
experiments, we examined mechanisms leading to neutrophil accumulation
and activation in the lungs after endotoxemia or hemorrhage. Levels of
IL-1ß, TNF-
, and macrophage inflammatory protein-2 mRNA were
increased in lung neutrophils from endotoxemic or hemorrhaged mice
compared with those present in lung neutrophils from control mice or in
peripheral blood neutrophils from endotoxemic, hemorrhaged, or control
mice. The transcriptional regulatory factors NF-
B and cAMP response
element binding protein were activated in lung but not blood
neutrophils after hemorrhage or endotoxemia. Xanthine oxidase
inhibition, achieved by feeding allopurinol or tungsten-containing
diets, did not affect neutrophil trafficking to the lungs after
hemorrhage or endotoxemia. Xanthine oxidase inhibition did prevent
hemorrhage- but not endotoxemia- induced increases in proinflammatory
cytokine expression among lung neutrophils. Hemorrhage- or
endotoxemia-associated activation of NF-B in lung neutrophils was
not affected by inhibition of xanthine oxidase. cAMP response element
binding protein activation was increased after hemorrhage, but not
endotoxemia, in mice fed xanthine oxidase-inhibiting diets. Our results
indicate that xanthine oxidase modulates cAMP response element binding
protein activation and proinflammatory cytokine expression in lung
neutrophils after hemorrhage, but not endotoxemia. These findings
suggest that the mechanisms leading to acute inflammatory lung injury
after hemorrhage differ from those associated with
endotoxemia.
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