Sulfatide attenuates experimental Staphylococcal aureus sepsis through a CD1d-dependent pathway

• Published in: Infection and immunity Vol. 81; no. 4; p. 1114
• Main Authors: Kwiecinski, Jakub, Rhost, Sara, Löfbom, Linda, Blomqvist, Maria K., Månsson, Jan-Eric, Cardell, Susanna, Jin, Tao
• Format: Journal Article
• Language: English
• Published: 2013
• Subjects: animal experiment; animal model; bacterial growth; cell survival; controlled study; female; Immunologi inom det medicinska området; Immunology in the medical area; Infectious Medicine; Infektionsmedicin; inoculation; lethality; mouse; natural killer T cell; nonhuman; priority journal; staphylococcal bacteremia; Staphylococcus aureus; survival rate; treatment outcome
• ISSN: 1098-5522
• DOI: 10.1128/IAI.01334-12

Natural 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 of Staphylococcus aureus sepsis. Lack of CD1d-restricted NKT cells did not alter survival after a lethal inoculum of S. aureus. In contrast, sulfatide treatment significantly improved the survival rate of mice with S. aureus sepsis, accompanied by decreased levels of TNF-α and IL-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 of S. aureus sepsis in this model.