Journal
INFECTION AND IMMUNITY
Volume 81, Issue 4, Pages 1114-1120Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.01334-12
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Funding
- Goteborg Medical Society
- Swedish Medical Society
- Rune and Ulla Amlovs Foundation
- Ake-Wiberg Foundation
- Tholens and Kristlers Family Foundation
- Tore Nilsons Foundation
- Swedish Rheumatism Association
- Goteborg Rheumatism Association
- Strategic Research Center for Mucosal Immunobiology and Vaccines (MIVAC)
- Swedish Cancer Foundation [CAN2010/793]
- Swedish Research Council [K2010-57X-14063-10-3]
- LUA-ALF Goteborg [ALF-GBG-151251]
- W. and M. Lundgrens Foundation
- Sahlgrenska Academy, University of Gothenburg
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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. The 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 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 of S. aureus sepsis in this model.
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