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

Journal article
Authors Jakub Kwiecinski
Sara Rhost
Linda Löfbom
Maria K. Blomqvist
Jan-Eric Månsson
Susanna Cardell
Tao Jin
Published in Infection and immunity
Volume 81
Issue 4
Pages 1114-1120
ISSN 1098-5522
Publication year 2013
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Institute of Biomedicine, Department of Microbiology and Immunology
Pages 1114-1120
Language en
Links dx.doi.org/10.1128/IAI.01334-12
https://gup.ub.gu.se/file/100999
Keywords animal experiment, animal model, article, bacterial growth, cell survival, controlled study, female, inoculation, lethality, mouse, natural killer T cell, nonhuman, priority journal, staphylococcal bacteremia, Staphylococcus aureus, survival rate, treatment outcome
Subject categories Immunobiology, Infectious Medicine

Abstract

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.

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