Angiostrongylus cantonensis is a metastrongyloid nematode that causes eosinophilic meningoencephalitis in humans. A high infestation of A. cantonensis can cause permanent brain damage or even death. The inflammasome is an oligomeric molecular platform that can detect microbial pathogens and activate inflammatory cytokines. The recognition of larval surface antigens by pattern recognition receptors (PRRs) can cause oligomerization of the NOD-like receptor (NLR) or absent in melanoma 2 (AIM2) with the adaptor apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) to form a caspase-1-activating scaffold. Activated caspase-1 converts pro-inflammatory cytokines into their mature, active forms. Helminths infection has been shown to activate NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasomes. In this study, we aimed to investigate the mechanism of inflammasome activation upon A. cantonensis infection in a mouse model. This study provides evidence that A. cantonensis infection can activate NLRP1B and NLRC4 inflammasomes and promote pyroptosis to cause meningoencephalitis.

广东血管圆线虫是一种会引起人类嗜酸性粒细胞性脑膜炎的间线粒状线虫。广州曲霉高发可能导致永久性脑损伤甚至死亡。炎性小体是可检测微生物病原体并激活炎性细胞因子的寡聚分子平台。模式识别受体（PRR）对幼虫表面抗原的识别可导致NOD样受体（NLR）寡聚或在黑色素瘤2（AIM2）中缺失，而适配器凋亡相关的斑点样蛋白含有胱天蛋白酶募集结构域（ASC） ）形成caspase-1激活支架。活化的caspase-1将促炎性细胞因子转化为成熟的活性形式。蠕虫感染已显示可激活NACHT，LRR和PYD结构域的蛋白3（NLRP3）炎性小体。在这项研究中，我们旨在研究广州烟曲霉炎性体激活的机制。小鼠模型感染。这项研究提供了证据，表明广州曲霉感染可以激活NLRP1B和NLRC4炎性小体并促进发烧而引起脑膜脑炎。