As Toll-like receptor 4 (TLR4) is the LPS-receptor on neutrophils (24), LPS-induced acute inflammation tissue injury models represent not just endotoxemia, but also represent sterile TLR4-activation by its endogenous ligand, S100A8/A9, an exemplar damage associated molecular pattern (DAMP) increased in acute lung injury which sustains neutrophil activation (25). This evidence concerns the gene TLR4 and injury.