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Transcriptomic Profiling of Mouse Mast Cells upon Pathogenic Avian H5N1 and Pandemic H1N1 Influenza a Virus Infection

文献类型： 外文期刊

作者： Tang, Yuling 1 ; Wu, Hongping 1 ; Huo, Caiyun 2 ; Zou, Shumei 3 ; Hu, Yanxin 1 ; Yang, Hanchun 1 ;

作者机构： 1.China Agr Univ, Coll Vet Med, Minist Agr, Key Lab Anim Epidemiol, Beijing 100193, Peoples R China

2.Beijing Acad Agr & Forestry Sci, Inst Anim Husb & Vet Med, Beijing Key Lab Prevent & Control Infect Dis Live, Beijing 100097, Peoples R China

3.Natl Inst Viral Dis Control & Prevent, Natl Hlth & Family Planning Commiss, Key Lab Med Virol,Chinese Ctr Dis Control & Preve, Collaborat Innovat Ctr Diag & Treatment Infect Di, Beijing 100013, Peoples R China

关键词： influenza A virus; Nbeal2; mast cell; transcriptome

期刊名称：VIRUSES-BASEL （ 影响因子：5.818； 五年影响因子：5.811 ）

ISSN：

年卷期： 2022 年 14 卷 2 期

页码：

收录情况： SCI

摘要： Mast cells, widely residing in connective tissues and on mucosal surfaces, play significant roles in battling against influenza A viruses. To gain further insights into the host cellular responses of mouse mast cells with influenza A virus infection, such as the highly pathogenic avian influenza A virus H5N1 and the human pandemic influenza A H1N1, we employed high-throughput RNA sequencing to identify differentially expressed genes (DEGs) and related signaling pathways. Our data revealed that H1N1-infected mouse mast P815 cells presented more up- and down-regulated genes compared with H5N1-infected cells. Gene ontology analysis showed that the up-regulated genes in H1N1 infection were enriched for more degranulation-related cellular component terms and immune recognition-related molecular functions terms, while the up-regulated genes in H5N1 infection were enriched for more immune-response-related biological processes. Network enrichment of the KEGG pathway analysis showed that DEGs in H1N1 infection were specifically enriched for the FoxO and autophagy pathways. In contrast, DEGs in H5N1 infection were specifically enriched for the NF-kappa B and necroptosis pathways. Interestingly, we found that Nbeal2 could be preferentially activated in H5N1-infected P815 cells, where the level of Nbeal2 increased dramatically but decreased in HIN1-infected P815 cells. Nbeal2 knockdown facilitated inflammatory cytokine release in both H1N1- and H5N1-infected P815 cells and aggravated the apoptosis of pulmonary epithelial cells. In summary, our data described a transcriptomic profile and bioinformatic characterization of H1N-1 or H5N1-infected mast cells and, for the first time, established the crucial role of Nbeal2 during influenza A virus infection.

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