Mycoplasma hyopneumoniae-derived lipid-associated membrane proteins induce inflammation and apoptosis in porcine peripheral blood mononuclear cells in vitro
Mycoplasma hyopneumoniae-derived lipid-associated membrane proteins induce inflammation and apoptosis in porcine peripheral blood mononuclear cells in vitro
复制标题
猪肺炎支原体衍生的脂质相关膜蛋白体外诱导猪外周血单核细胞炎症和凋亡
DOI：
10.1016/j.vetmic.2014.11.013
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发表时间：
2015-01-30
影响因子：
3.3
通讯作者：
Shao, Guoqing
中科院分区：
文献类型：
--
作者：
Bai, Fangfang;Ni, Bo;Shao, Guoqing
猪肺炎支原体（Mycoplasma hyopeptidase，Mycoplasma hyopeptidase，MP）是引起猪流行性肺炎（Swine enzootic pneumonia，EP）的病原体，是造成养猪业严重经济损失的主要原因。支原体的脂质相关膜蛋白（LAMPs）在引起支原体疾病中起重要作用。本研究旨在探讨M.通过阐明它们在调节猪外周血单个核细胞（PBMC）的炎症、凋亡和相关信号通路中的作用，来研究猪肺炎支原体LAMPs。LAMP处理抑制PBMC的生长。细胞因子如IL-6和IL-1 β的上调，以及一氧化氮（NO）和超氧阴离子的产生增加，都在LAMPs处理的PBMC的上清液中检测到。流式细胞术分析表明，用Annexin-V-FITC和碘化丙啶（PI）双重染色，M.结果表明，低聚果糖可诱导PBMC中淋巴细胞和单核细胞凋亡，且呈时间依赖性，NOS抑制剂或抗氧化剂可阻断低聚果糖诱导的PBMC中淋巴细胞和单核细胞凋亡。此外，LAMP诱导PBMC中p38的磷酸化、促凋亡Bax蛋白与抗凋亡Bcl-2蛋白的比例、caspase-3和caspase-8的活化以及聚ADP-核糖聚合酶（PARP）的裂解。这些结果表明M.体外实验表明，LPS通过p38 MAPK和Bax/Bcl-2信号通路以及caspase激活诱导PBMC产生促炎细胞因子NO和活性氧（ROS），并诱导PBMC凋亡。(C)2014爱思唯尔有限公司版权所有。
Mycoplasma hyopneumoniae is the causative agent of swine enzootic pneumonia (EP), a disease that causes considerable economic losss in swine industry. Lipid-associated membrane proteins (LAMPs) of mycoplasma play important roles in causing mycoplasma diseases. The present study explores the pathogenic mechanisms of M. hyopneumoniae LAMPs by elucidating their role in modulating the inflammation, apoptosis, and relevant signaling pathways of peripheral blood mononuclear cells (PBMCs) of pig. LAMP treatment inhibited the growth of PBMCs. Up-regulation of cytokines, such as IL-6 and IL-1 beta, as well as increased production of nitric oxide (NO) and superoxide anion were all detected in the supernatant of LAMPs-treated PBMCs. Furthermore, flow cytometric analysis using dual staining with annexin-V-FITC and propidium iodide (PI) showed that LAMPs of M. hyopneumoniae induced a time-dependent apoptosis in lymphocyts and monocytes from PBMCs, which was blocked by NOS inhibitor or antioxidant. In addition, LAMPs induced the phosphorylation of p38, the ratio of pro-apoptotic Bax protein to anti-apoptotic Bcl-2, activation of caspase-3 and caspase-8, and poly ADP-ribose polymerase (PARP) cleavage in PBMCs. These findings demonstrated that M. hyopneumoniae LAMPs induced the production of proinflammatory cytokines, NO and reactive oxygen species (ROS), and apoptosis of PBMCs in vitro through p38 MAPK and Bax/Bcl-2 signaling pathways, as well as caspase activation. (C) 2014 Elsevier B.V. All rights reserved.