Abnormal bacterial colonization and activation of innate immunity by lipopolysaccharide (LPS) probably have a role in the pathogenesis of necrotizing enterocolitis. In a rodent model of necrotizing enterocolitis, high concentrations of LPS-binding protein (LBP) promoted wound healing and decreased levels of TLR4 (a marker of inflammation). Futher studies are now warranted to investigate this potential therapeutic strategy.