PMN apoptosis is a crucial injurylimiting mechanism of inflammatory resolution. Circulating PMN undergo constitutive apoptosis that results in the shutdown of secretary capacity and allows PMN recognition and removal by macrophages (82, 83) . Several inflammatory agents, such as LPS, TNF, IL-8, IL-6, IL-1 and granulocyte colony-stimulating factor (G-CSF), can delay apoptotic response, providing PMN with a longer life span, which in turn allows the PMN to accumulate at local tissue sites of inflammation/infection (84, 85) . Protein 53 (p53) is a transcription factor that is important in multicellular organisms, where it regulates the cell cycle and promotes apoptosis. Modulation of p53 by nutlin-3α diminished the response of PMN and macrophages to stimulation through TLR2 or TLR4 as well as attenuated LPS-induced ALI. NF-κB has been reported as a modulator of apoptosis in inflammatory cells (86) . p53 can negatively regulate NF-κB activity by decreasing binding of NF-κB to the promoters of genes for proinflammatory cytokines. In p53 -/mice, the inflammatory process and severity of ALI in response to LPS are enhanced (87) .