HIV-1-derived exosomal microRNAs miR88 and miR99 promote the release of cytokines from human alveolar macrophages by binding to TLR8
Author(s) -
Zhao Hui,
Sun Zhenming,
Li Lifang,
Zhi Shuyin,
Zhao Yiru,
Zhang Zhihua,
Wang Runyu,
Li Jianqiang
Publication year - 2019
Publication title -
european journal of inflammation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.219
H-Index - 20
eISSN - 2058-7392
pISSN - 1721-727X
DOI - 10.1177/2058739219870434
Subject(s) - tumor necrosis factor alpha , immune system , immunology , microvesicles , macrophage , biology , cytokine , u937 cell , interleukin , in vitro , microbiology and biotechnology , microrna , biochemistry , gene
The human monocytic cell line U937 and human alveolar macrophages were used as in vitro models to explore the role of miR88 and miR99 in the chronic abnormal activation of the body caused by human immunodeficiency virus (HIV). The functions and underlying mechanisms of miR88 and miR99 were studied by real-time quantitative polymerase chain reaction, transwell, and chromatin immunoprecipitation (ChIP) assays. HIV-1-infected cells released miR88 and miR99 into the extracellular space through exosomes, and miR88 and miR99 promoted the release of tumor necrosis factor alpha (TNFα), interleukin (IL)-6, and IL-12 by activating inflammatory factors, such as TLR8, on the surface of macrophages. HIV-derived microRNAs miR88 and miR99 performed these functions by binding to TLR8 and stimulating the release of pro-inflammatory factors from macrophages, such as TNFα, IL-6, and IL-12; these factors may be involved in chronic abnormal immune activation induced by HIV infection.
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