PMN accumulation has been observed early in lung tissue (19, 20) as well as in bronchoalveolar lavage fluids (BALF) of ARDS patients (16) . When developed during neutropenia, ALI rapidly progressed once PMN counts were restored (21, 22) . Furthermore, the degree of neutrophilia in BALF has been correlated with poor prognosis in septic ARDS (23) . In an experimental setting of indirect ALI stemming from hemorrhagic shock (HEM) followed by polymicrobial sepsis, we found that, in response to HEM, circulating PMNs exhibited an ex vivo increase in respiratory burst capacity and a decrease in apoptosis. This is consistent with the concept that shock/injury can produce in vivo "priming," the significance of which could be seen when HEM then was followed by sepsis, as recruitment of these PMNs into the lung occurred, along with the development of ALI (24) . Also, when these HEM-primed PMNs were injected intravenously into PMN-depleted animals, which subsequently underwent cecal ligation and puncture (CLP) to induce sepsis, ALI again resulted (24) . Upon this background, using different models of ALI, we (25) and others (26) (27) (28) (29) (30) (31) (32) have found that depletion of PMNs actually may serve to decrease injury associated with ALI. Thus, depletion of PMNs prior to HEM and sepsis markedly reduced the extent of lung inflammation and ameliorated lung protein influx and the severity of ALI (25) , which is in line with findings during transfusion-induced ALI (29) .