Endotoxin, septic shock and acute lung injury: neutrophils, macrophages and inflammatory mediators.
The treatment of septic shock remains a major problem in surgical practice. Current research on the pathogenesis of the sepsis syndrome focuses on the effects of the lipopolysaccharide constituents of bacterial endotoxin. Evidence suggests that endotoxin induces a whole-body inflammatory response that in turn mediates organ damage, eventually leading to multiorgan failure. The first organ in which failure is usually apparent is the lung, with the appearance of non-cardiogenic pulmonary oedema as part of the adult respiratory distress syndrome. Inflammatory cells involved in lung injury include neutrophils and macrophages, which release mediators such as elastase, oxygen radicals and cytokines. This review summarizes current experimental work on how endotoxin leads to lung injury, based on its effects in animals and patients. Present knowledge suggests that future treatment of septic shock might involve inhibiting the body's inflammatory response to endotoxin. Possible ways of doing this are discussed.
Welbourn
C R
CR
Department of Surgery, Stepping Hill Hospital, Stockport, London, UK.
Young
Y
Y
D004731:Endotoxins / Q000494:pharmacology*; D006801:Humans; D007249:Inflammation; D009504:Neutrophils / Q000187:drug effects / Q000502:physiology*; D012128:Respiratory Distress Syndrome / Q000209:etiology* / Q000628:therapy; D012772:Shock, Septic / Q000209:etiology* / Q000628:therapy
D004731:Endotoxins