ARDS is one of the most serious complications in critically ill septic patients. Many studies have pointed out a role for oxidative stress in ARDS and shown a protective effect of GSH precursors. 80, 81 Most of the studies of ARDS in animal models, including those cited above, are based on the administration of lipopolysaccharide (LPS), a bacterial endotoxin. In mice, administration of LPS induces an acute lung injury similar to clinical ARDS, with production of inflammatory cytokines, leukocyte infiltration in the lung, and pulmonary edema. In this model, various thiol-based antioxidants are protective. [80] [81] [82] However, LPS administration is in fact a model of endotoxic shock, involving no live bacteria, to induce a state similar to what was once called septic shock and is now defined as systemic inflammatory response syndrome. [83] [84] [85] However, in septic patients, survival is affected by 2 opposite contributions of innate immunity: innate immunity is detrimental as systemic inflammation, which results in ARDS and shock, but on the other hand it is an essential component of the immune defense against infection. It is difficult to foresee how GSH affects this balance.