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长非编码 RNA 谱分析显示,LncRNA BTN3A2 抑制了鸡对 的宿主炎症反应。

Long noncoding RNA profiling reveals that LncRNA BTN3A2 inhibits the host inflammatory response to infection in chickens.

机构信息

College of Animal Science and Technology, Yangzhou University, Yangzhou, China.

Poultry Institute, Chinese Academy of Agricultural Sciences, Yangzhou, China.

出版信息

Front Immunol. 2022 Aug 25;13:891001. doi: 10.3389/fimmu.2022.891001. eCollection 2022.

DOI:10.3389/fimmu.2022.891001
PMID:36091044
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9452752/
Abstract

Coccidiosis is a widespread parasitic disease that causes serious economic losses to the poultry industry every year. Long noncoding RNAs (lncRNAs) play important roles in transcriptional regulation and are involved in a variety of diseases and immune responses. However, the lncRNAs associated with () resistance have not been identified in chickens. In addition, the expression profiles and functions of lncRNAs during infection remain unclear. In the present study, high-throughput sequencing was applied to identify lncRNAs in chicken cecal tissues from control (JC), resistant (JR), and susceptible (JS) groups on day 4.5 post-infection (pi), and functional tests were performed. A total of 564 lncRNAs were differentially expressed, including 263 lncRNAs between the JS and JC groups, 192 between the JR and JS groups, and 109 between the JR and JC groups. Functional analyses indicated that these differentially expressed lncRNAs were involved in pathways related to infection, including the NF-kappa B signaling, B cell receptor signaling and natural killer cell-mediated cytotoxicity pathways. Moreover, through cis regulation network analysis of the differentially expressed lncRNAs, we found that a novel lncRNA termed lncRNA BTN3A2 was significantly increased in both cecum tissue and DF-1 cells after coccidia infection or sporozoite stimulation. Functional test data showed that the overexpression of lncRNA BTN3A2 reduced the production of inflammatory cytokines, including IL-6, IL-1β, TNF-α and IL-8, while lncRNA BTN3A2 knockdown promoted the production of these inflammatory cytokines. Taken together, this study identify the differentially expressed lncRNAs during infection in chickens for the first time and provide the direct evidence that lncRNA BTN3A2 regulates the host immune response to coccidia infection.

摘要

球虫病是一种广泛存在的寄生虫病,每年都会给家禽养殖业造成严重的经济损失。长链非编码 RNA(lncRNA)在转录调控中发挥着重要作用,并参与多种疾病和免疫反应。然而,鸡中与()抗性相关的 lncRNA 尚未被鉴定。此外,lncRNA 在()感染过程中的表达谱和功能尚不清楚。在本研究中,我们采用高通量测序技术在感染后第 4.5 天(pi)鉴定了来自对照组(JC)、抗性组(JR)和易感组(JS)鸡盲肠组织中的 lncRNA,进行了功能测试。共鉴定到 564 个差异表达的 lncRNA,其中 JS 与 JC 组之间有 263 个 lncRNA,JR 与 JS 组之间有 192 个 lncRNA,JR 与 JC 组之间有 109 个 lncRNA。功能分析表明,这些差异表达的 lncRNA 参与了与感染相关的途径,包括 NF-kappa B 信号通路、B 细胞受体信号通路和自然杀伤细胞介导的细胞毒性通路。此外,通过差异表达 lncRNA 的顺式调控网络分析,我们发现一种新型 lncRNA,称为 lncRNA BTN3A2,在球虫感染或裂殖子刺激后,在盲肠组织和 DF-1 细胞中均显著增加。功能测试数据表明,lncRNA BTN3A2 的过表达降低了炎症细胞因子(包括 IL-6、IL-1β、TNF-α 和 IL-8)的产生,而 lncRNA BTN3A2 的敲低则促进了这些炎症细胞因子的产生。总之,本研究首次鉴定了鸡感染过程中的差异表达 lncRNA,并提供了直接证据表明 lncRNA BTN3A2 调节宿主对球虫感染的免疫反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2997/9452752/8af6908f8e55/fimmu-13-891001-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2997/9452752/75304467353d/fimmu-13-891001-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2997/9452752/fe089183b59e/fimmu-13-891001-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2997/9452752/4366810baa89/fimmu-13-891001-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2997/9452752/0be7d763a58a/fimmu-13-891001-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2997/9452752/fd1a3332771a/fimmu-13-891001-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2997/9452752/8af6908f8e55/fimmu-13-891001-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2997/9452752/75304467353d/fimmu-13-891001-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2997/9452752/b36eab36b527/fimmu-13-891001-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2997/9452752/53435d4a39c4/fimmu-13-891001-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2997/9452752/f673118a72ae/fimmu-13-891001-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2997/9452752/fe089183b59e/fimmu-13-891001-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2997/9452752/4366810baa89/fimmu-13-891001-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2997/9452752/0be7d763a58a/fimmu-13-891001-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2997/9452752/fd1a3332771a/fimmu-13-891001-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2997/9452752/8af6908f8e55/fimmu-13-891001-g009.jpg

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