Alveolar macrophage activation after XXXX and @entity295 is dependent on NF-kappaB and MAPK/ERK mechanisms.

@entity558 @entity295 @entity548 @entity649 @entity568 @entity4 @entity1505 @entity35 @entity860 @entity1589 @entity130 @entity17104
The @entity649 ( @entity649 ) is a major cause of morbidity after injury. We hypothesized that alveolar macrophage (AMPhi) chemokine and cytokine release after @entity548 and @entity295 is regulated by NF-kappaB and MAPK. Adult male @entity35 underwent soft tissue @entity130 and @entity548 (~90 min) followed by crystalloid resuscitation. @entity295 was induced by cecal ligation and puncture (CLP) 20 h after resuscitation. @entity860 hi were harvested, and @entity1505 , @entity568 , and @entity17104 release and serum @entity568 and @entity1505 levels were measured at 5 h after HCLP. Lung tissues were analyzed for activation of NF-kappaB, @entity1589 activity, and wet/dry weight ratio. In control animals, @entity860 hi were stimulated with @entity558 with or without inhibitors of NF-kappaB and MAPK. Serum @entity1505 and @entity568 levels and spontaneous @entity860 hi @entity1505 and @entity17104 release were elevated (P < 0.05) after HCLP, concomitantly with the development of @entity4 and leukocyte activation. Activation of NF-kappaB increased in lungs from the @entity548 and CLP group compared with shams. Inhibition of NF-kappaB or the upstream MAPK significantly decreased @entity558 -stimulated AMPhi activation. Because enhanced release of inflammatory mediators by AMPhi may contribute to @entity649 after severe @entity130 , inhibition of intracellular signaling pathways represents a target to attenuate organ injury under those conditions.
