Sulfatide Attenuates Experimental Staphylococcus aureus Sepsis through a CD1d-Dependent Pathway

Abstract

ABSTRACTNatural killer T (NKT) lymphocytes are implicated in the early response to microbial infection. Further, sulfatide, a myelin self-glycosphingolipid, activates a type II NKT cell subset and can modulate disease in murine models. We examined the role of NKT cells and the effect of sulfatide treatment in a murine model ofStaphylococcus aureussepsis. The lack of CD1d-restricted NKT cells did not alter survival after a lethal inoculum ofS. aureus. In contrast, sulfatide treatment significantly improved the survival rate of mice withS. aureussepsis, accompanied by decreased levels of tumor necrosis factor alpha and interleukin-6 in the blood. The protective effect of sulfatide treatment depended on CD1d but not on type I NKT cells, suggesting that activation of type II NKT cells by sulfatide has beneficial effects on the outcome ofS. aureussepsis in this model.