Extensive PMN influx into the lungs is one of the characteristics of ALI. Studies have shown that excessive induction of proinflammatory cytokines in PMN and delayed PMN apoptosis are associated with higher mortality and more severe organ dysfunction in sepsis patients (72, 73) . Human PMN express all TLR mRNA except TLR3. TLR2 are more abundant than TLR4 on PMN (74, 75) . PMN recruitment to the lung after LPS inhalation is primarily dependent on TLR4-NF-κB signaling (76, 77) . The PI3K/Akt pathway was also reported to be involved in TLR4-induced expression of IL-1β, TNF-α and chemokine macro phage inflammatory protein (MIP)-2 (78) .