A balanced game: chicken macrophage response to ALV-J infection

文献类型： 外文期刊

第一作者： Feng, Min

作者： Feng, Min;Xie, Tingting;Li, Yuanfang;Zhang, Nan;Lu, Qiuyuan;Zhou, Yaohong;Sun, Jingchen;Zhang, Xiquan;Xie, Tingting;Li, Yuanfang;Zhang, Xiquan;Shi, Meiqing

作者机构：

期刊名称：VETERINARY RESEARCH （ 影响因子：3.683； 五年影响因子：4.106 ）

ISSN： 0928-4249

年卷期： 2019 年 50 卷

页码：

收录情况： SCI

摘要： Avian leukosis virus subgroup J (ALV-J) infection can cause tumors and immunosuppression in infected chickens. Macrophages play a central role in host defense against invading pathogens. In this study, we discovered an interesting phenomenon: ALV-J replication is weakened from 3hours post-infection (hpi) to 36hpi, which was verified using Western blotting and RT-PCR. To further investigate the interaction between ALV-J and macrophages, transcriptome analysis was performed to analyze the host genes' function in chicken primary monocyte-derived macrophages (MDM). Compared to the uninfected control, 624 up-regulated differentially expressed genes (DEG) and 341 down-regulated DEG at 3 hpi, and 174 up-regulated DEG and 87 down-regulated DEG at 36 hpi were identified in chicken MDM, respectively. ALV-J infection induced strong innate immune responses in chicken MDM at 3 hpi, instead of 36 hpi, according to the analysis results of Gene Ontology and KEGG pathway. Importantly, the host factors, such as up-regulated MIP-3, IL-1, iNOS, K60, IRG1, CH25H, NFKBIZ, lysozyme and OASL were involved in the host defense response during the course of ALV-J infection. On the contrary, up-regulated EX-FABP, IL4I1, COX-2, NFKBIA, TNFAIP3 and the Jak STAT pathway inhibitors including CISH, SOCS1 and SOCS3 are beneficial to ALV-J survival in chicken macrophages. We speculated that ALV-J tropism for macrophages helps to establish a latent infection in chicken MDM from 6 to 36 hpi. The present study provides a comprehensive view of the interactions between macrophages and ALV-J. It suggests the mechanisms of defense of chicken macrophages against ALV-J invasion and how ALV-J escape the host innate immune responses.

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