NKT Cells: The Culprits of Sepsis?

Leung, Briana; Harris, Hobart W.

doi:10.1016/j.jss.2010.09.038

Cited by 19 publications

(17 citation statements)

References 88 publications

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“…The hyperreactive phase is characterized by a potentially fatal cytokine storm induced by activated monocytes, macrophages, and other immune cells. Previous studies are consistent with a role for NKT cells in the early response to microbial infection, demonstrating that type I NKT cells can contribute to lipopolysaccharide (LPS)-induced endotoxic shock and Gram-negative sepsis (19). Mice lacking type I NKT cells had lower levels of circulating gamma interferon (IFN-␥) and TNF-␣ and increased survival in the generalized Shwartzman reaction (20).…”

Section: Figmentioning

confidence: 55%

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

et al. 2013

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Natural killer T (NKT) lymphocytes are implicated in the early response to microbial infection. Further, sulfatide, a myelin selfglycosphingolipid, 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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Section: Figmentioning

confidence: 55%

“…Due to their contribution to microbial immunity and their rapid response to activation, NKT cells were proposed to have a role in sepsis and endotoxic shock (19). Initial studies pointed to a detrimental role of NKT cells in sepsis by magnifying damage and increasing mortality (20)(21)(22)(23)(24).…”

mentioning

confidence: 99%

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

et al. 2013

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“…Regarding the role of NKT cells in sepsis, there are competing opinions: one is that NKT cells are involved in harmful outcomes in sepsis as reviewed by Leung and Harris [43], and another is that those cells exhibit a protective function in sepsis [44,45]. Thus, it becomes important to explain such a discrepancy.…”

Section: Resultsmentioning

confidence: 99%

Galectin-9 prolongs the survival of septic mice by expanding tim-3-expressing natural killer T cells and PDCA-1+ CD11c+ macrophages

et al. 2013

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IntroductionGalectin-9 ameliorates various inflammatory conditions including autoimmune diseases by regulating T cell and macrophage/dendritic cell (DC) functions. However, the effect of galectin-9 on polymicrobial sepsis has not been assessed.MethodsWe induced polymicrobial sepsis by cecal ligation and puncture (CLP) in mice. The survival rate was compared between galectin-9- and PBS-treated CLP mice. An ELISA was used to compare the levels of various cytokines in the plasma and culture supernatants. Fluorescence-activated cell sorting analysis was further performed to compare the frequencies of subpopulations of spleen cells.ResultsGalectin-9 exhibited a protective effect in polymicrobial sepsis as demonstrated in galetin-9 transgenic mice and therapeutic galectin-9 administration. In contrast, such effect was not observed in nude mice, indicating the involvement of T cells in galectin-9-mediated survival prolongation. Galectin-9 decreased TNFα, IL-6, IL-10 and, high mobility group box 1 (HMGB1) and increased IL-15 and IL-17 plasma and spleen levels. Galectin-9 increased the frequencies of natural killer T (NKT) cells and PDCA-1+ CD11c+ macrophages (pDC-like macrophages) but did not change the frequency of CD4 or CD8 T cells, γδT cells or conventional DC. As expected, galectin-9 decreased the frequency of Tim-3+ CD4 T cells, most likely Th1 and Th17 cells. Intriguingly, many spleen NK1.1+ NKT cells and pDC-like macrophages expressed Tim-3. Galectin-9 increased the frequency of Tim-3-expressing NK1.1+ NKT cells and pDC-like macrophages. Galectin-9 further increased IL-17+ NK1.1+ NKT cells.ConclusionThese data suggest that galectin-9 exerts therapeutic effects on polymicrobial sepsis, possibly by expanding NKT cells and pDC-like macrophages and by modulating the production of early and late proinflammatory cytokines.

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“…Thus, depletion of NK cells results in attenuation of inflammatory reaction and an overall improvement in outcome. [37] Therefore, NK cells can be considered as important targets for therapeutic strategies. Depletion of NK cells in a murine polytrauma model is associated with improved outcome and a modulation of the infl ammatory response.…”

Section: Hmgb1 and Nk Cellsmentioning

confidence: 99%

Novel insights for high mobility group box 1 protein-mediated cellular immune response in sepsis:A systemic review

Huang¹,

Yao²,

Zhang³

2012

World Journal of Emergency Medicine

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NKT Cells: The Culprits of Sepsis?

Cited by 19 publications

References 88 publications

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

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

Galectin-9 prolongs the survival of septic mice by expanding tim-3-expressing natural killer T cells and PDCA-1+ CD11c+ macrophages

Novel insights for high mobility group box 1 protein-mediated cellular immune response in sepsis:A systemic review

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