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Immunological pathways of macrophage response to Brucella ovis infection
Innate Immunity ( IF 2.8 ) Pub Date : 2020-09-24 , DOI: 10.1177/1753425920958179
Zhixiong Zhou 1 , Guojing Gu 1 , Yichen Luo 1, 2, 3 , Wenjie Li 1 , Bowen Li 1 , Yu Zhao 1 , Juan Liu 1, 2, 3 , Xuehong Shuai 1, 2, 3 , Li Wu 1, 3 , Jixuan Chen 1, 3 , Cailiang Fan 1, 4 , Qingzhou Huang 1, 3 , Baoru Han 5 , Jianjun Wen 6 , Hanwei Jiao 1, 2, 3
Affiliation  

As the molecular mechanisms of Brucella ovis pathogenicity are not completely clear, we have applied a transcriptome approach to identify the differentially expressed genes (DEGs) in RAW264.7 macrophage infected with B. ovis. The DEGs related to immune pathway were identified by Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) functional enrichment analysis. Quantitative real-time PCR (qRT-PCR) was performed to validate the transcriptome sequencing data. In total, we identified 337 up-regulated and 264 down-regulated DEGs in B. ovis-infected group versus mock group. Top 20 pathways were enriched by KEGG analysis and 20 GO by functional enrichment analysis in DEGs involved in the molecular function, cellular component, and biological process and so on, which revealed multiple immunological pathways in RAW264.7 macrophage cells in response to B. ovis infection, including inflammatory response, immune system process, immune response, cytokine activity, chemotaxis, chemokine-mediated signaling pathway, chemokine activity, and CCR chemokine receptor binding. qRT-PCR results showed Ccl2 (ENSMUST00000000193), Ccl2 (ENSMUST00000124479), Ccl3 (ENSMUST00000001008), Hmox1 (ENSMUST00000005548), Hmox1 (ENSMUST00000159631), Cxcl2 (ENSMUST00000075433), Cxcl2 (ENSMUST00000200681), Cxcl2 (ENSMUST00000200919), and Cxcl2 (ENSMUST00000202317). Our findings firstly elucidate the pathways involved in B. ovis-induced host immune response, which may lay the foundation for revealing the bacteria–host interaction and demonstrating the pathogenic mechanism of B. ovis.



中文翻译:

巨噬细胞对绵羊布鲁氏菌感染的免疫通路

由于绵羊布鲁氏菌致病性的分子机制尚不完全清楚,我们应用转录组方法来鉴定感染了绵羊布鲁氏菌的RAW264.7 巨噬细胞中的差异表达基因 (DEG) 。通过京都基因和基因组百科全书(KEGG)和基因本体论(GO)功能富集分析鉴定了与免疫通路相关的DEG。进行定量实时 PCR (qRT-PCR) 以验证转录组测序数据。我们总共在B. ovis 中鉴定了 337 个上调和 264 个下调的 DEG- 感染组与模拟组。通过KEGG分析富集了前20条通路,通过功能富集分析富集了20条GO,涉及分子功能、细胞成分、生物学过程等DEGs,揭示了RAW264.7巨噬细胞响应B. ovis的多重免疫通路感染,包括炎症反应、免疫系统过程、免疫反应、细胞因子活性、趋化性、趋化因子介导的信号通路、趋化因子活性和CCR趋化因子受体结合。定量RT-PCR结果显示CCL2(ENSMUST00000000193),CCL2(ENSMUST00000124479)CCL3(ENSMUST00000001008)HMOX1(ENSMUST00000005548)HMOX1(ENSMUST00000159631),CXCL2(ENSMUST00000075433),CXCL2(ENSMUST00000200681),CXCL2(ENSMUST00000200919)和CXCL2(ENSMUST00000202317)。我们的研究结果首先阐明了B. ovis诱导宿主免疫反应的途径,这可能为揭示B. ovis的细菌-宿主相互作用和阐明B. ovis的致病机制奠定基础。

更新日期:2020-09-24
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