Chen T T W, Cheng P C, Chang K C, Cao J P, Feng J L, Chen C C, Lam H Y P, Peng S Y
Department of Biochemistry, School of Medicine, Tzu Chi University, Hualien 97004, Taiwan.
National Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention; Key Laboratory of Parasite and Vector Biology, MOH, Shanghai 200025, China.
J Helminthol. 2019 Aug 15;94:e72. doi: 10.1017/S0022149X19000622.
Schistosomiasis is an inflammatory disease that occurs when schistosome species eggs are deposited in the liver, resulting in fibrosis and portal hypertension. Schistosomes can interact with host inflammasomes to elicit host immune responses, leading to mitochondrial damage, generation of high levels of reactive oxygen species (ROS) and activation of apoptosis during inflammation. This study aims to examine whether ROS and NF-κB (p65) expression elicited other types of inflammasome activation in Schistosoma mansoni-infected mouse livers. We examine the relationship between inflammasome activation, mitochondrial damage and ROS production in mouse livers infected with S. mansoni. We demonstrate a significant release of ROS and superoxides and increased NF-κB (p65) in S. mansoni-infected mouse livers. Moreover, activation of the NLRP3 and AIM2 inflammasomes was triggered by S. mansoni infection. Stimulation of HuH-7 hepatocellular carcinoma cells with soluble egg antigen induced activation of the AIM2 inflammasome pathway. In this study, we demonstrate that S. mansoni infection promotes both NLRP3 and AIM2 inflammasome activation.
血吸虫病是一种炎症性疾病，当血吸虫虫卵沉积在肝脏时就会发生，导致肝纤维化和门静脉高压。血吸虫可与宿主炎性小体相互作用，引发宿主免疫反应，导致线粒体损伤、大量活性氧（ROS）生成以及炎症期间细胞凋亡的激活。本研究旨在探讨ROS和NF-κB（p65）表达是否会引发曼氏血吸虫感染小鼠肝脏中其他类型的炎性小体激活。我们研究了曼氏血吸虫感染小鼠肝脏中炎性小体激活、线粒体损伤与ROS产生之间的关系。我们证明，曼氏血吸虫感染的小鼠肝脏中ROS和超氧化物大量释放，NF-κB（p65）增加。此外，曼氏血吸虫感染触发了NLRP3和AIM2炎性小体的激活。用可溶性虫卵抗原刺激HuH-7肝癌细胞可诱导AIM2炎性小体途径的激活。在本研究中，我们证明曼氏血吸虫感染促进了NLRP3和AIM2炎性小体的激活。
