دورية أكاديمية
أعرض في EDS

The hijacking of HBV by small extracellular vesicles inhibits M1 macrophages to facilitate immune evasion.

التفاصيل البيبلوغرافية
العنوان: The hijacking of HBV by small extracellular vesicles inhibits M1 macrophages to facilitate immune evasion.
المؤلفون: Zhang Z; Institute of Basic Medicine and Forensic Medicine, North Sichuan Medical College, Nanchong, 637000, China.; Xichong County People's Hospital, Nanchong, 637200, Sichuan, China., Liu J; The Third Hospital of Mianyang, Sichuan Mental Health Center, Mianyang, 621000, China., Yu L; Institute of Basic Medicine and Forensic Medicine, North Sichuan Medical College, Nanchong, 637000, China., Zeng R; Institute of Basic Medicine and Forensic Medicine, North Sichuan Medical College, Nanchong, 637000, China., Pan W; Institute of Basic Medicine and Forensic Medicine, North Sichuan Medical College, Nanchong, 637000, China. panwl@aliyun.com.
المصدر: Scientific reports [Sci Rep] 2024 Aug 27; Vol. 14 (1), pp. 19917. Date of Electronic Publication: 2024 Aug 27.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Nature Publishing Group Country of Publication: England NLM ID: 101563288 Publication Model: Electronic Cited Medium: Internet ISSN: 2045-2322 (Electronic) Linking ISSN: 20452322 NLM ISO Abbreviation: Sci Rep Subsets: MEDLINE
أسماء مطبوعة: Original Publication: London : Nature Publishing Group, copyright 2011-
مواضيع طبية MeSH: Extracellular Vesicles*/metabolism , Extracellular Vesicles*/immunology , Hepatitis B virus*/immunology , Macrophages*/immunology , Macrophages*/metabolism , Macrophages*/virology , MicroRNAs*/genetics , MicroRNAs*/metabolism , Hepatitis B*/virology , Hepatitis B*/immunology , Hepatitis B*/metabolism , Immune Evasion*, Humans ; Hep G2 Cells ; Toll-Like Receptor 4/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; Interleukin-18/metabolism ; THP-1 Cells
مستخلص: Small extracellular vesicles (sEVs) have the ability to transfer genetic material between cells, but their role in mediating HBV infection and regulating M1 macrophages to promote immune evasion remains unclear. In this study, we utilized PMA + LPS + IFN-γ to induce THP-1 into M1 macrophages. We then extracted sEVs from HepG2.2.15 cell and treated the M1 macrophages with these sEVs. QPCR detection revealed the presence of HBV-DNA in the M1 macrophages. Additionally, RT-qPCR and WB analysis demonstrated a significantly decreased in the expression of TLR4, NLRP3, pro-caspase-1, caspase-1p20, IL-1β and IL-18 in the M1 macrophages (P < 0.05). Furthermore, RT-qPCR results displayed high expression levels of that miR-146a and FEN-1 in the sEVs derived from HepG2.2.15 cells (P < 0.01). RT -qPCR and WB analysis showed that these sEVs enhanced the expression of FEN-1 or miR-146a in the M1 macrophages through miR-146a or FEN-1 (P < 0.05), while simultaneously reducing the expression of TLR4, NLRP3, caspase-1p20, IL-1β and IL-18 in the M1 macrophages (P < 0.05). In summary, our findings indicate that sEVs loaded with HBV inhibit the inflammatory function of M1 macrophages and promote immune escape. Additionally, miR-146a and FEN-1 present in the sEVs play a crucial role in this process.
(© 2024. The Author(s).)
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فهرسة مساهمة: Keywords: FEN-1; Immune evasion; M1 macrophages; MiR-146a; Small extracellular vesicles
المشرفين على المادة: 0 (MicroRNAs)
0 (Toll-Like Receptor 4)
0 (MIRN146 microRNA, human)
0 (NLR Family, Pyrin Domain-Containing 3 Protein)
0 (Interleukin-18)
تواريخ الأحداث: Date Created: 20240828 Date Completed: 20240828 Latest Revision: 20240903
رمز التحديث: 20240903
مُعرف محوري في PubMed: PMC11358331
DOI: 10.1038/s41598-024-70924-3
PMID: 39198597
قاعدة البيانات: MEDLINE
الوصف
تدمد:2045-2322
DOI:10.1038/s41598-024-70924-3