We appreciate Dr. Fujita's valuable input regarding an animal model of chronic endotoxemia and the role of regulatory T cells (Tregs) in liver disease. Cani and colleagues recently reported that a high-fat diet increases plasma lipopolysaccharide (LPS) level. 1 Chronic infusion of LPS in mice fed a normal diet causes a metabolic response similar to high-fat feeding, including obesity, insulin resistance, and increased liver triglyceride content. In this sense, the high-fat diet mouse model that we use represents a model of chronic endotoxemia. Our acute exogenous LPS experiments merely reflect an exacerbated inflammatory status that helped us to determine the role of Tregs in modulation of hepatic inflammation under a fatty liver condition. 2 Tregs express several members of Toll-like receptors (TLR). Exposing Tregs to LPS induces up-regulation of several activation markers and enhances Treg survival and proliferation. 3 In addition, LPS treatment increases Treg suppression efficiency in vitro and in vivo. Therefore, it will be interesting to compare the number and the function of hepatic Tregs in the model of chronic exogenous LPS infusion to the model of high-fat diet-induced fatty liver disease.