IL-33 缺乏可通过促进 NLRP3 炎性体抑制弓形虫感染。

IF 1.8 3区 医学 Q2 PARASITOLOGY
Yizhong Chen, Xiaoli He, Yuqin Chen, Rongzhao Zhang, Tengwen Zhang, Tao Zhang, Linqing Wu
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引用次数: 0

摘要

NLRP3 炎性体介导的炎症反应在先天性免疫中发挥着关键作用。然而,人们对它的平衡调控仍有待进一步了解。在此,我们通过一系列分子生物学和免疫学实验,包括Western blot、qRT-PCR和ELISA,探讨了弓形虫感染后IL-33对NLRP3炎性体的影响和潜在机制。我们发现弓形虫感染会诱导IL-33的表达,而IL-33缺陷型(IL-33-/-)小鼠在感染弓形虫后的存活时间比野生型(WT)小鼠更长。IL-33缺乏会促进NLRP3和ASC的表达以及IL-1β的分泌,而外源IL-33会抑制NLRP3炎性体。此外,淋球菌感染会导致巨噬细胞的M2极化,而外源性IL-33会加剧这种极化,这也会促进淋球菌的增殖。这些研究结果表明,缺乏IL-33可通过促进NLRP3炎性体减轻淋球菌感染,从而加深了人们对IL-33在炎症中作用的理解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
IL-33 deficiency inhibits Toxoplasma gondii infection by promoting NLRP3 inflammasome.

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.

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来源期刊
Parasitology Research
Parasitology Research 医学-寄生虫学
CiteScore
4.10
自引率
5.00%
发文量
346
审稿时长
6 months
期刊介绍: The journal Parasitology Research covers the latest developments in parasitology across a variety of disciplines, including biology, medicine and veterinary medicine. Among many topics discussed are chemotherapy and control of parasitic disease, and the relationship of host and parasite. Other coverage includes: Protozoology, Helminthology, Entomology; Morphology (incl. Pathomorphology, Ultrastructure); Biochemistry, Physiology including Pathophysiology; Parasite-Host-Relationships including Immunology and Host Specificity; life history, ecology and epidemiology; and Diagnosis, Chemotherapy and Control of Parasitic Diseases.
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