As eluded to above, chemokines are critically involved in the activation and recruitment of PMNs to the lung, potentially contributing to their harmful effects on an organ level. In this regard, associations between chemokines, lung neutrophil influx, and alveolo-capillary dysfunction have been reported (63, 64) . In our experiments, we observed that during hemorrhage-induced septic ALI (24) , as well as after experimental blunt chest trauma (65) , chemokines are markedly upregulated locally in the lung of the animals, as well as systemically. Blockade of the CXCR (chemokine [CXC motif] receptor) 2 using antileukinate, a hexapeptide inhibitor, following HEM, reduced lung PMN influx in response to subsequent sepsis and additionally decreased lung inflammation and lung protein leak, while pulmonary IL-10 levels were markedly increased (66) . We also administered anti-KC or anti-MIP-2 antibody into mice immediately following HEM. The adoptive transfer of PMN isolated from the anti-MIP, but not from the anti-KC-treated donors, exhibited a reduction of lung inflammation and lung PMN influx in the recipients in response to sepsis when compared with control Ig-treated donors (67) . These data demonstrated that hemorrhage-induced priming of PMNs not only mediated experimental ALI, but also that this process was differentially effected by MIP-2 and KC, although both signal through CXCR2 in mice. However, as humans utilize IL-8 in place of the two mouse α-chemokines and because receptors for IL-8, i.e. CXCR1 and CXCR2, also are utilized differently, these murine chemokine data may not translate directly to the patient setting of ALI/ARDS (68) .