{"title":"IL-33 缺乏可通过促进 NLRP3 炎性体抑制弓形虫感染。","authors":"Yizhong Chen, Xiaoli He, Yuqin Chen, Rongzhao Zhang, Tengwen Zhang, Tao Zhang, Linqing Wu","doi":"10.1007/s00436-024-08414-8","DOIUrl":null,"url":null,"abstract":"<p><p>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<sup>-/-</sup>) 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.</p>","PeriodicalId":19968,"journal":{"name":"Parasitology Research","volume":"123 11","pages":"391"},"PeriodicalIF":1.8000,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"IL-33 deficiency inhibits Toxoplasma gondii infection by promoting NLRP3 inflammasome.\",\"authors\":\"Yizhong Chen, Xiaoli He, Yuqin Chen, Rongzhao Zhang, Tengwen Zhang, Tao Zhang, Linqing Wu\",\"doi\":\"10.1007/s00436-024-08414-8\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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<sup>-/-</sup>) 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.</p>\",\"PeriodicalId\":19968,\"journal\":{\"name\":\"Parasitology Research\",\"volume\":\"123 11\",\"pages\":\"391\"},\"PeriodicalIF\":1.8000,\"publicationDate\":\"2024-11-21\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Parasitology Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/s00436-024-08414-8\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"PARASITOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Parasitology Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s00436-024-08414-8","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"PARASITOLOGY","Score":null,"Total":0}
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.
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.