Li Siqi, Chen Tianfeng, Gao Kexin, Yang Yong-Bo, Qi Baojie, Wang Chunsheng, An Tongqing, Cai Xuehui, Wang Shujie
State Key Laboratory for Animal Disease Control and Prevention, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin 150001, China.
College of Life Science, Northeast Forestry University, Harbin 150040, China.
Microorganisms. 2024 Sep 12;12(9):1879. doi: 10.3390/microorganisms12091879.
is an important bacterial pathogen that affects the global pig industry. The immunosuppressive nature of infection is recognized, and our previous research has confirmed thymus atrophy with a large number of necrotic cells. In this current work, we aimed to uncover the role of pyroptosis in cellular necrosis in thymic cells of -infected mice. Confocal microscopy revealed that activated the M1 phenotype and primed pyroptosis in the macrophages of atrophied thymus. Live cell imaging further confirmed that could induce porcine alveolar macrophage (PAM) pyroptosis in vitro, displaying cell swelling and forming large bubbles on the plasma membrane. Meanwhile, the levels of p-p38, p-extracellular signal-regulated kinase (ERK) and protein kinase B (AKT) were increased, which indicated the mitogen-activated protein kinase (MAPK) and AKT pathways were also involved in the inflammation of -infected PAMs. Furthermore, RT-PCR revealed significant mRNA expression of pro-inflammatory mediators, including interleukin (IL)-1β, IL-6, IL-18, tumor necrosis factor (TNF)-α and chemokine CXCL8. The data indicated that the inflammation induced by was in parallel with pro-inflammatory activities of M1 macrophages, pyroptosis and MAPK and AKT pathways. Pyroptosis contributes to necrotic cells and thymocyte reduction in the atrophied thymus of mice.
是一种影响全球养猪业的重要细菌病原体。人们认识到感染具有免疫抑制特性，我们之前的研究已证实胸腺萎缩伴有大量坏死细胞。在当前这项工作中，我们旨在揭示焦亡在感染小鼠胸腺细胞坏死中的作用。共聚焦显微镜显示，激活了萎缩胸腺巨噬细胞中的M1表型并引发焦亡。活细胞成像进一步证实，可在体外诱导猪肺泡巨噬细胞（PAM）焦亡，表现为细胞肿胀并在质膜上形成大气泡。同时，p-p38、p-细胞外信号调节激酶（ERK）和蛋白激酶B（AKT）的水平升高，这表明丝裂原活化蛋白激酶（MAPK）和AKT信号通路也参与了感染PAM的炎症反应。此外，逆转录聚合酶链反应（RT-PCR）显示促炎介质白细胞介素（IL）-1β、IL-6、IL-18、肿瘤坏死因子（TNF）-α和趋化因子CXCL8的mRNA表达显著。数据表明，诱导的炎症反应与M1巨噬细胞的促炎活性、焦亡以及MAPK和AKT信号通路并行。焦亡导致小鼠萎缩胸腺中的坏死细胞和胸腺细胞减少。
