Mycoplasma ovipneumoniae induces inflammatory response in sheep airway epithelial cells via a MyD88-dependent TLR signaling pathway
Mycoplasma ovipneumoniae induces inflammatory response in sheep airway epithelial cells via a MyD88-dependent TLR signaling pathway
复制标题
绵羊肺炎支原体通过 MyD88 依赖性 TLR 信号通路诱导绵羊气道上皮细胞炎症反应
DOI：
10.1016/j.vetimm.2014.11.008
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发表时间：
2015-01-15
影响因子：
1.8
通讯作者：
Wang, Yujiong
中科院分区：
文献类型：
--
作者：
Xue, Di;Ma, Yan;Wang, Yujiong
绵羊肺炎支原体（M.绵羊肺炎（ovinepneumoniae）是一种特异性感染绵羊和山羊并引起绵羊传染性胸膜肺炎的细菌。为了了解病原菌与宿主之间的相互作用，对M.为了研究绵羊肺炎病毒（ovipneumoniae，ovipneumoniae）与气道上皮细胞的相互作用，我们采用宁夏滩羊（Ovisaries）支气管上皮细胞原代气液界面（air-liquidinterface，ALI）上皮细胞培养模型，研究了宿主的炎症反应。羊支气管上皮细胞的ALI培养显示出完全分化的上皮，包括不同的上皮类型，包括基底细胞、纤毛细胞和杯状细胞。将ALI培养物暴露于M.绵羊肺炎导致Toll样受体（TLR）和髓样分化因子88（MyD 88）依赖性TLR信号传导途径的组分（包括MyD 88、TNF受体相关因子6（TRAF 6）、IL-1受体相关激酶（IRAKs）和核因子-κ B（NF-κ B））以及随后的上皮细胞中的促炎细胞因子的表达增加。有趣的是，感染M。ovipneumoniae未能诱导TANK结合激酶1（TBK 1）、TRAF 3和干扰素调节因子3（IRF 3）的表达，这些是MyD 88非依赖性信号通路的关键组分。这些结果表明，MyD 88依赖性TLR途径可能在绵羊气道上皮细胞对M.这也表明ALI培养系统可能是研究绵羊肺炎支原体与病原宿主相互作用的可靠模型。绵羊肺炎和气道上皮细胞。(C)2014爱思唯尔有限公司版权所有。
Mycoplasma ovipneumoniae (M. ovipneumoniae) is a bacterium that specifically infects sheep and goat and causes ovine infectious pleuropneumonia. In an effort to understand the pathogen host interaction between the M. ovipneumoniae and airway epithelial cells, we investigated the host inflammatory response using a primary air liquid interface (ALI) epithelial culture model generated from bronchial epithelial cells of Ningxia Tan sheep (Ovis aries). The ALI culture of sheep bronchial epithelial cells showed a fully differentiated epithelium comprising distinct epithelial types, including the basal, ciliated and goblet cells. Exposure of ALI cultures to M. ovipneumoniae led to increased expression of Toll-like receptors (TLRs), and components of the myeloid differentiation factor 88 (MyD88)-dependent TLR signaling pathway, including the MyD88, TNF receptor-associated factor 6 (TRAF6), IL-1 receptor-associated kinases (IRAKs) and nuclear factor-kappa B (NF-kappa B), as well as subsequent pro-inflammatory cytokines in the epithelial cells. Of interest, infection with M. ovipneumoniae failed to induce the expression of TANK-binding kinase 1 (TBK1), TRAF3 and interferon regulatory factor 3 (IRF3), key components of the MyD88-independent signaling pathway. These results suggest that the MyD88-dependent TLR pathway may play a crucial role in sheep airway epithelial cells in response to M. ovipneumoniae infection, which also indicate that the ALI culture system may be a reliable model for investigating pathogen host interactions between M. ovipneumoniae and airway epithelial cells. (C) 2014 Elsevier B.V. All rights reserved.