Xue Di, Ma Yan, Li Min, Li Yanan, Luo Haixia, Liu Xiaoming, Wang Yujiong
Key Laboratory of Ministry of Education for Conservation and Utilization of Special Biological Resources in the Western China, China; College of Life Science, Ningxia University, Yinchuan, Ningxia 750021, China.
Key Laboratory of Ministry of Education for Conservation and Utilization of Special Biological Resources in the Western China, China; College of Life Science, Ningxia University, Yinchuan, Ningxia 750021, China.
Vet Immunol Immunopathol. 2015 Jan 15;163(1-2):57-66. doi: 10.1016/j.vetimm.2014.11.008. Epub 2014 Nov 20.
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-κB), 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.
绵羊肺炎支原体是一种专门感染绵羊和山羊并引起绵羊传染性胸膜肺炎的细菌。为了了解绵羊肺炎支原体与气道上皮细胞之间的病原体-宿主相互作用，我们使用从宁夏滩羊支气管上皮细胞生成的原代气液界面（ALI）上皮培养模型研究了宿主炎症反应。绵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，如基底细胞、纤毛细胞和杯状细胞。将ALI培养物暴露于绵羊肺炎支原体后，Toll样受体（TLR）以及髓样分化因子88（MyD88）依赖性TLR信号通路的成分，包括MyD88、肿瘤坏死因子受体相关因子6（TRAF6）、白细胞介素-1受体相关激酶（IRAKs）和核因子-κB（NF-κB）的表达增加，随后上皮细胞中促炎细胞因子也增加。有趣的是，感染绵羊肺炎支原体未能诱导MyD88非依赖性信号通路的关键成分TANK结合激酶1（TBK1）、TRAF3和干扰素调节因子3（IRF3）的表达。这些结果表明，MyD88依赖性TLR途径可能在绵羊气道上皮细胞对绵羊肺炎支原体感染的反应中起关键作用，这也表明ALI培养系统可能是研究绵羊肺炎支原体与气道上皮细胞之间病原体-宿主相互作用的可靠模型。
Zotero 插件