IL-33 deficiency inhibits Toxoplasma gondii infection by promoting NLRP3 inflammasome.

Autor: Chen Y; The Department of Immunology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China., He X; The Department of Immunology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China., Chen Y; The Department of Immunology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China., Zhang R; The Department of Immunology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China., Zhang T; The Department of Immunology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China., Zhang T; The Department of Immunology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China. zjdrzht@fjmu.edu.cn., Wu L; The Department of Immunology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China. wu_linqing@hotmail.com.
Jazyk: angličtina
Zdroj: Parasitology research [Parasitol Res] 2024 Nov 21; Vol. 123 (11), pp. 391. Date of Electronic Publication: 2024 Nov 21.
DOI: 10.1007/s00436-024-08414-8
Abstrakt: NLRP3 inflammasome-mediated inflammatory responses play pivotal functions in innate immunity. However, its homeostatic regulation still needs to be better understood. Here we explore the effect and potential mechanism of IL-33 on NLRP3 inflammasome upon Toxoplasma gondii infection through a series of molecular biology and immunological experiments, including western blot, qRT-PCR, and ELISA. We demonstrated that T. gondii infection induces the expression of IL-33, and IL-33-deficient (IL-33 -/- ) mice exhibit longer survival time than wild-type (WT) mice upon T. gondii infection. IL-33 deficiency promotes the expression of NLRP3 and ASC and the secretion of IL-1β, while exogenous IL-33 inhibits NLRP3 inflammasome. Furthermore, T. gondii infection results in the M2 polarization of macrophages, exacerbated by exogenous IL-33, which also promotes the proliferation of T. gondii. These findings showed that IL-33 deficiency attenuates T. gondii infection by promoting NLRP3 inflammasome, advancing the understanding of the role of IL-33 in inflammation.
Competing Interests: Declarations. Ethical approval: Animal procedures were conducted under the “Guiding Principles in the Care and Use of Animals” (China) and were approved by the Laboratory Animal Ethics Committee of Fujian Medical University (FJMU IACUC 2019–0144). Consent for publication: All authors agree to publish. Competing interests: The authors declare no competing interests.
(© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)
Databáze: MEDLINE
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