Skin lipopolysaccharide-binding protein and IL-1 beta production after thermal injury

In response to a burn injury, skill can have an inflammatory response chara cterized by the production of inflammatory cytokines, recruitment of immune cells, containment of invading organisms, and clearance of noxious substan ces from the wound. Lipopolysaccharide-binding protein (LBP) is a molecule that is capable of coordinating all 4 functions; we previously found eviden ce that suggested that LBP is produced within surgical wounds. Because of t he central role of LBP in the response to bacterial infection, as well as i n the high rate of infection after burn injuries, we sought to determine wh ether a thermal injury could affect wound LBP production and thereby affect host responses against bacterial infection. Rats were given either a burn or a sham burn and were killed 24, 48, and 72 hours after the injuries. Wou nd specimens were assayed for bacterial counts and for the presence of LBP, messenger (m)RNA, and interleukin (IL)-1 beta mRNA. Wound LBP mRNA was sig nificantly upregulated at 24 hours in the group with burn injuries (P < .05 ; burn vs sham burn); this was followed by decreases at 48 and 72 hours. Im munohistochemistry showed LBP protein in the epidermis of animals with burn s. Bacterial counts increased in the group with burn injuries (P < .05; bur n vs sham burn) and continued to rise for 72 hours. IL-1 beta mRNA levels w ere elevated at all time points in the group with burn injuries (P < .05). These results suggest an inverse correlation between burn wound LBP express ion and bacterial wound counts. This failure to maintain local LBP producti on after severe thermal injury despite localized inflammation shown by high IL-1 beta levels may predispose local wounds to bacterial invasion.