IL-33 attenuates mortality by promoting IFN-γ production in sepsis
Objective and design
Sepsis remains a major clinical problem with high morbidity and mortality. Interleukin (IL)-33 is a recently described member of the IL-1 family that is widely expressed and functions as a new inflammatory mediator. IL-33 has been reported to protect sepsis, but the underlying mechanisms are not well-elucidated.
Materials and methods
We measured the interferon gamma (IFN-γ) production in septic mice after IL-33 treatment.
IL-33 treatment enhanced the IFN-γ level in blood and promoted mice’s survival, so the protective effects of IL-33 depend on IFN-γ. The IL-33 treatment also promoted both γδ T cells and NK cells in septic mice.
Our data showed that IL-33 attenuates mortality by promoting IFN-γ production in sepsis.
KeywordsIL-33 IFN-γ γδ T cells NK cells Sepsis
Compliance with ethical standards
Conflict of interest
The authors declare that they have no conflict of interest.
Research involving human participants and/or animals
All applicable international, national, and/or institutional guidelines for the care and use of animals were followed.
- 6.LaRosa SP, Opal SM. Sepsis strategies in development. Clin Chest Med. 2008;29(4):735–47, x–xi.Google Scholar
- 10.Crispe IN. Isolation of mouse intrahepatic lymphocytes. Curr Protoc Immunol. 2001;Chap. 3(Unit 3):21.Google Scholar
- 18.Wang Y, Kong BB, Yang WP, Zhao X, Zhang R. Immunomodulatory intervention with gamma interferon in mice with sepsis. Life Sci. 2017;18585–94.Google Scholar