We used a simplified animal model of the two-hit paradigm to address the mechanisms of HS-primed PMN migration and lung inflammation (114) . In this model, animals are subjected to a nonsevere resuscitated HS (hypotension at 40 mmHg for 1 hour, followed by a small dose of intratracheal LPS. Although neither shock nor LPS alone induces injury, the combination caused lung PMN accumulation and increased 125 I-albumin transpulmonary flux. Findings from this model have suggested that the mechanisms underlying the priming of PMN and inflammation involve a complicated receptor cross-talk process and interaction between PMN and AMφ, which is described below.