Capsular Polysaccharide is a Main Component of Mycoplasma ovipneumoniae in the Pathogen-Induced Toll-Like Receptor-Mediated Inflammatory Responses in Sheep Airway Epithelial Cells.
Capsular Polysaccharide is a Main Component of Mycoplasma ovipneumoniae in the Pathogen-Induced Toll-Like Receptor-Mediated Inflammatory Responses in Sheep Airway Epithelial Cells.
复制标题
荚膜多糖是绵羊气道上皮细胞病原体诱导的 Toll 样受体介导的炎症反应中绵羊肺炎支原体的主要成分
DOI：
10.1155/2017/9891673
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发表时间：
2017
影响因子：
4.6
通讯作者：
Wang Y
中科院分区：
文献类型：
--
作者：
Jiang Z;Song F;Li Y;Xue D;Deng G;Li M;Liu X;Wang Y
卵肺炎支原体（M. ovipneumoniae）的特点是原发性非典型肺炎的病原，特异性感染绵羊和山羊。为了更好地了解入侵的卵肺炎支原体与气道上皮细胞之间的病原-宿主相互作用，我们利用在气液界面（ALI）模型中培养的绵羊支气管上皮细胞，研究了宿主对卵肺炎支原体荚膜多糖（CPS）的炎症反应。结果表明，产自卵肺炎支原体的CPS可激活toll样受体- (TLR-)介导的炎症反应，同时提高核因子κB （NF-κB）、激活蛋白-1 （AP-1）、干扰素调节因子3 （IRF3）以及各种炎症相关介质的表达，包括促炎因子如IL1β、TNFα和IL8，以及抗炎因子如IL10和TGFβ。从机制上讲，cps诱导的炎症是TLR启动的，并通过myd88依赖性和myd88非依赖性信号通路的激活介导。重要的是，用特异性抗体阻断CPS导致绵羊支气管上皮细胞中肺炎支原体诱导的炎症反应显著减少。这些结果表明，CPS是肺炎支原体的关键毒力成分，可能在肺炎支原体感染引起的炎症反应中起关键作用。
Mycoplasma ovipneumoniae (M. ovipneumoniae) is characterized as an etiological agent of primary atypical pneumonia that specifically infects sheep and goat. In an attempt to better understand the pathogen-host interaction between the invading M. ovipneumoniae and airway epithelial cells, we investigated the host inflammatory responses against capsular polysaccharide (designated as CPS) of M. ovipneumoniae using sheep bronchial epithelial cells cultured in an air-liquid interface (ALI) model. Results showed that CPS derived from M. ovipneumoniae could activate toll-like receptor- (TLR-) mediated inflammatory responses, along with an elevated expression of nuclear factor kappa B (NF-κB), activator protein-1 (AP-1), and interferon regulatory factor 3 (IRF3) as well as various inflammatory-associated mediators, representatively including proinflammatory cytokines, such as IL1β, TNFα, and IL8, and anti-inflammatory cytokines such as IL10 and TGFβ of TLR signaling cascade. Mechanistically, the CPS-induced inflammation was TLR initiated and was mediated by activations of both MyD88-dependent and MyD88-independent signaling pathways. Of importance, a blockage of CPS with specific antibody led a significant reduction of M. ovipneumoniae-induced inflammatory responses in sheep bronchial epithelial cells. These results suggested that CPS is a key virulent component of M. ovipneumoniae, which may play a crucial role in the inflammatory response induced by M. ovipneumoniae infections.