In our model of hemorrhage-induced septic ALI, it was evident that prolonging the lifespan of activated PMNs by using transgenic mice that overexpress the anti-apoptotic protein Bcl-2 in a myeloid-restricted fashion (95) did not exacerbate acute lung injury, although a prolonged presence of activated PMNs in the lung was evident (96) . In contrast, we observed an initial survival benefit when the life span of PMNs was further prolonged, likely due to an enhanced capacity to clear bacteria as evidenced by the lower bacteria counts in the lung (96) . In addition, in an inflammatory/ non-infectious environment, such as SIRS, mimicked by intraperitoneal injection of E. coli-LPS, prolonging the lifespan of activated PMNs was detrimental for the animals' survival and was associated with an exacerbation of lung injury (96) . Additionally, during non-infectious/ inflammatory ALI, failure to clear PMNs from the lungs contributed to increased inflammation and mortality (97) . Together, these data imply that the tissue environment (infectious versus inflammatory) that the neutrophil encounters plays an important role in determining whether PMNs mediate organ damage or not. However, the mechanisms which determine whether PMN turn bad or good are not understood well and require further investigation.