We have used this model to study the role of endogenous GSH in sepsis. 86 In this model, CLP induced PMN infiltration in the peritoneal cavity, the site of infection, as well as in the lung, ultimately resulting in lung injury and death, with a concomitant decrease in endogenous GSH. 86 Lowering GSH further with BSO worsened the clinical settings. Not only did BSO increase PMN infiltrate in the lung, but it also diminished PMN infiltration in the site of infection, thus increasing bacterial growth. As a result we had more inflammation and less immunity, and survival was dramatically decreased. Repleting GSH with NAC had the opposite effect of reducing PMN infiltration to the lung but increasing that to the site of infection, thus decreasing bacterial colonies.