Seki Takenori, Obata-Ninomiya Kazushige, Shimogawara-Furushima Rieko, Arai Toshio, Akao Nobuaki, Hoshino Tomoaki, Ohta Nobuo
Department of Environmental Parasitology, Tokyo Medical and Dental University, Tokyo, Japan.
Department of Environmental Parasitology, Tokyo Medical and Dental University, Tokyo, Japan; Department of Immune Regulation, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
Parasitol Int. 2018 Feb;67(1):64-69. doi: 10.1016/j.parint.2017.03.008. Epub 2017 Mar 27.
It has been reported that IL-33 contributes to potentiation of Th2 inflammatory diseases and protection against helminth infection. Increased plasma IL-33 levels have been observed in patients with severe falciparum malaria, however, the role of IL-33 in malaria remains unclear. Here we report that IL-33 enhances inflammatory responses in malaria infection. ST2-deficiency altered severity of inflammation in the liver and serum levels of pro-inflammatory cytokines such as TNF-α and IL-6, and IL-13 that is a Th2 cytokine during Plasmodium chabaudi infection. IL-13-deficient mice have similar phenotype with ST2-deficient mice during P. chabaudi infection. Furthermore, ST2- and IL-13-deficiency reduced mortality from P. chabaudi infection. These results indicate that IL-33/ST2 can induce production of proinflammatory cytokines, such as TNF-α and IL-6, through production of IL-13 in P. chabaudi-infected BALB/c mice, suggesting that IL-33/ST2 play a critical role in inflammatory responses to malaria infection. Thus, these findings may define a novel therapeutic target for patients with severe malaria.
据报道，白细胞介素-33（IL-33）有助于增强Th2炎症性疾病，并对蠕虫感染具有保护作用。在重症恶性疟患者中观察到血浆IL-33水平升高，然而，IL-33在疟疾中的作用仍不清楚。在此我们报告，IL-33可增强疟疾感染中的炎症反应。在感染恰氏疟原虫期间，ST2缺陷改变了肝脏炎症的严重程度以及促炎细胞因子如肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-
