Tian Wei, Zhao Chengcheng, Hu Qingchuang, Sun Jianjun, Peng Xiuli
Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction, Ministry of Education, Huazhong Agricultural University, Wuhan 430070, China.
Department of Biological Sciences and Border Biomedical Research Center, University of Texas at El Paso, El Paso, TX 79968, USA.
Dev Comp Immunol. 2016 Jun;59:39-47. doi: 10.1016/j.dci.2016.01.008. Epub 2016 Jan 19.
While Mycoplasma gallisepticum (MG) is a major pathogen that causes chronic respiratory diseases in chicken, the molecular mechanism of MG infection is not clear. In this study, we investigated the roles of Toll-like receptor 2 (TLR2) and 6 (TLR6) in MG infection. We found that TLR2 type 2 (TLR2-2) and TLR6 had differential expressions in chicken embryo fibroblasts (DF-1 cells), where TLR6 was highly expressed, but TLR2-2 was barely expressed. Upon MG infection, TLR6 expression was upregulated, followed by upregulation of downstream factors, MyD88, NF-κB, IL2, IL6, and TNF-α. Knockdown of TLR6 expression by shRNA abolished the MG-induced inflammatory responses. More interestingly, in the presence of TLR6, TLR2-2 didn't respond to MG infection in DF-1 cells. When TLR6 was knocked down by shRNA, however, TLR2 was upregulated upon MG infection, which was followed by upregulation of proinflammatory genes. Finally, we tested effects of the MG infection on expression of TLR2-2 and TLR6 in the lungs and trachea tissues of chicken embryos. We found both TLR2-2 and TLR6 were upregulated upon MG infection, followed by upregulation of the downstream NF-κB-mediated inflammatory responses. This study was the first to report the differential roles of TLR2-2 and TLR6 in MG-infected DF-1 cells and chicken embryos.
虽然鸡毒支原体(MG)是导致鸡慢性呼吸道疾病的主要病原体,但其感染的分子机制尚不清楚。在本研究中,我们调查了Toll样受体2(TLR2)和6(TLR6)在MG感染中的作用。我们发现TLR2的2型(TLR2-2)和TLR6在鸡胚成纤维细胞(DF-1细胞)中有差异表达,其中TLR6高表达,而TLR2-2几乎不表达。MG感染后,TLR6表达上调,随后下游因子MyD88、NF-κB、IL2、IL6和TNF-α也上调。通过shRNA敲低TLR6表达消除了MG诱导的炎症反应。更有趣的是,在存在TLR6的情况下,TLR2-2在DF-1细胞中对MG感染无反应。然而,当通过shRNA敲低TLR6时,MG感染后TLR2上调,随后促炎基因上调。最后,我们测试了MG感染对鸡胚肺和气管组织中TLR2-2和TLR6表达的影响。我们发现MG感染后TLR2-2和TLR6均上调,随后下游NF-κB介导的炎症反应上调。本研究首次报道了TLR2-2和TLR6在MG感染的DF-1细胞和鸡胚中的不同作用。