Il-33/st2 contributes to severe symptoms in plasmodium chabaudi-infected balb/c mice
Il-33/st2 contributes to severe symptoms in plasmodium chabaudi-infected balb/c mice
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Il-33/st2 导致感染恰鲍迪疟原虫的 balb/c 小鼠出现严重症状
DOI：
10.1016/j.parint.2017.03.008
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发表时间：
2017
影响因子：
1.9
通讯作者：
Ohta N.
中科院分区：
文献类型：
--
作者：
Seki T;Obata-Ninomiya K;Shimogawara-Furushima R;Arai T;Akao N;Hoshino T;Ohta N.
据报道，IL-33有助于增强Th 2炎性疾病和保护免受蠕虫感染。在严重恶性疟疾患者中观察到血浆IL-33水平升高，然而，IL-33在疟疾中的作用仍不清楚。在这里，我们报告说，IL-33增强疟疾感染的炎症反应。ST 2缺乏改变了肝脏炎症的严重程度和促炎细胞因子如TNF-α和IL-6的血清水平，以及在疟原虫感染期间作为Th 2细胞因子的IL-13。IL-13缺陷小鼠在P.沙鲍迪感染此外，ST-2和IL-13缺乏降低了P.沙鲍迪感染提示IL-33/ST 2可通过诱导P细胞产生IL-13而诱导TNF-α和IL-6等促炎细胞因子的产生。Chabaudi感染的BALB/c小鼠，表明IL-33/ST 2在疟疾感染的炎症反应中起关键作用。因此，这些发现可能为严重疟疾患者定义一个新的治疗靶点。
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 duringPlasmodium chabaudiinfection. IL-13-deficient mice have similar phenotype with ST2-deficient mice duringP. chabaudiinfection. Furthermore, ST2- and IL-13-deficiency reduced mortality fromP. chabaudiinfection. 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 inP. 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.