HEMORRHAGIC-SHOCK INDUCES G-CSF EXPRESSION IN BRONCHIAL EPITHELIUM

Hemorrhagic shock (HS) initiates a series of inflammatory processes th at includes the activation of polymorphonuclear granulocytic neutrophi ls (PMN). We tested the hypothesis that HS induces granulocyte colony- stimulating factor (G-CSF), a cytokine that augments PMN effector func tions, in the lungs of rats. Sprague-Dawley rats were subjected to com pensated or decompensated HS followed by resuscitation and death at 4 or 8 h. Animals subjected to HS demonstrated acute lung injury with PM N infiltration, edema, and hypoxia. Using semiquantitative reverse tra nscriptase-polymerase chain reaction, we detected a 1.9- to 7.1-fold i ncrease in G-CSF mRNA levels in the lung of animals subjected to HS co mpared with sham controls. Levels of G-CSF mRNA increased with increas ed duration of the ischemic phase of resuscitated shock. In situ hybri dization revealed that bronchoepithelial cells were the major cellular site of G-CSF mRNA. Thus production of G-CSF mRNA by bronchoepithelia l cells is dramatically increased in a rat model of HS that also demon strated lung injury. Increased local G-CSF levels may contribute to PM N recruitment and activation and resultant lung injury in HS.