College of Animal Science and Technology, Shihezi University, Shihezi, Xinjiang 832003, China.
College of Animal Science and Technology, Shihezi University, Shihezi, Xinjiang 832003, China.
Res Vet Sci. 2020 Oct;132:57-68. doi: 10.1016/j.rvsc.2020.05.014. Epub 2020 May 21.
An experiment was conducted to reveal why the Argali hybrid sheep are susceptible to Mycoplasma ovipneumoniae infection, the causative agent of mycoplasma ovipneumonia, a chronic respiratory disease that is harmful to the sheep industry.
After nine Argali hybrid sheep, divided into three groups, were experimentally infected with an M. ovipneumoniae strain at 0, 4 and 14 days, transcriptome profiling of lung tissues was performed by deep RNA sequencing, using the Illumina platform. Analysis of differentially expressed genes was performed to determine concomitant gene-specific temporal patterns of mRNA expression in the lungs after M. ovipneumoniae infection. 156 differentially expressed genes (44 up-regulated, 112 down-regulated) were found when comparing transcriptomic data at 4 and 0 days post-infection, and 367 (35 up-regulated, 332 down-regulated) when comparing 14 versus 0 days post-infection. Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that the differentially expressed genes at 4 and 14 versus 0 days post-infection were enriched in 109 and 150 pathways, respectively, and the Primary immunodeficiency pathway was considered most closely related to MO infection (p < .01). Hyper-IgM syndrome was identified based on the B-cell Immunodeficiency signaling pathway from differentially expressed genes related to M. ovipneumoniae infection. Gene Ontology analysis showed that differentially expressed genes in different groups were enriched for 497 and 928 terms, where those most closely related to M. ovipneumoniae infection are ciliated motor damage (p < .01).
The situation that ciliary movement is significantly inhibited and B cells in immunodeficiency are possibly the most important reason why Argali hybrid sheep are susceptible to MO.
本实验旨在揭示为何盘羊杂交羊易感染绵羊肺炎支原体(导致绵羊支原体肺炎的病原体),这是一种对绵羊养殖业有害的慢性呼吸道疾病。
将 9 只盘羊杂交羊分为 3 组,在 0、4 和 14 天分别用绵羊肺炎支原体株进行人工感染,然后用 Illumina 平台进行深度 RNA 测序,对肺组织进行转录组谱分析。通过分析差异表达基因,确定绵羊肺炎支原体感染后肺组织中基因特异性的 mRNA 表达的伴随时间模式。在比较感染后 4 天和 0 天的转录组数据时,发现了 156 个差异表达基因(44 个上调,112 个下调),在比较感染后 14 天和 0 天的转录组数据时,发现了 367 个差异表达基因(35 个上调,332 个下调)。京都基因与基因组百科全书通路分析表明,在感染后 4 天和 14 天与 0 天相比,差异表达基因分别富集在 109 和 150 条通路上,原发性免疫缺陷途径被认为与 MO 感染最密切相关(p<.01)。根据与绵羊肺炎支原体感染相关的差异表达基因,鉴定出 B 细胞免疫缺陷信号通路中的高 IgM 综合征。基因本体论分析表明,不同组中的差异表达基因分别富集了 497 和 928 个术语,其中与绵羊肺炎支原体感染最密切相关的术语是纤毛运动损伤(p<.01)。
纤毛运动受到显著抑制,免疫缺陷中的 B 细胞可能是盘羊杂交羊易感染 MO 的最重要原因。