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Transmembrane TNF-α Reverse Signaling Alleviates Lipopolysaccharide-induced Inflammation by Regulating the MCPIP1/SIRT1/NF-κB Pathway | ||
| Iranian Journal of Immunology | ||
| دوره 22، شماره 1، خرداد 2025، صفحه 13-24 اصل مقاله (1.9 M) | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.22034/iji.2025.104371.2907 | ||
| نویسندگان | ||
| Chenxi Li؛ Mingxin Lin؛ Xiujuan Li؛ Lijin Chen؛ Yubin Lin؛ Huiming Ye* | ||
| Department of Laboratory Medicine, Fujian Key Clinical Specialty of Laboratory Medicine, Women and Children’s Hospital, School of Medicine, Xiamen University, Xiamen, Fujian, China | ||
| چکیده | ||
| Background: Studies have demonstrated that transmembrane tumor necrosis factor-α (tmTNF-α) plays an anti-inflammatory role. tmTNF-α has a dual function, acting as both a signaling ligand and a receptor that transmits reverse signaling to cells expressing tmTNF-α. However, the role and mechanisms of tmTNF-α reverse signaling in sepsis are not fully understood. Objective: To explore the potential role and mechanisms of tmTNF-α reverse signaling in lipopolysaccharide (LPS)-induced inflammation. Methods: The expression levels of tmTNF-α and TNF-α mRNA were evaluated using flow cytometry and real-time PCR, respectively. We employed the anti-TNF-α drug infliximab to stimulate tmTNF-α reverse signaling and measured interleukin-6 (IL-6) and monocyte chemoattractant protein (MCP)-1 production through real-time PCR and ELISA in THP-1-derived macrophages. The location of p65 was determined through immunofluorescence assay. The phosphorylation and acetylation of p65, as well as the expression levels of MCP-induced protein 1 (MCPIP1) and Sirtuin 1 (SIRT1), were evaluated using western blotting. Results: Our findings revealed that tmTNF-α reverse signaling reduced the expression of IL-6 and MCP-1 triggered by LPS. tmTNF-α reverse signaling inhibited the nuclear translocation of p65, suppressed p65 phosphorylation and acetylation, and upregulated the expression of negative regulatory molecules MCPIP1 and SIRT1 in the LPS/ toll-like receptor 4 (TLR4) signaling pathway. Conclusion: This study demonstrates that tmTNF-α reverse signaling plays a negative regulatory role in inflammation triggered by LPS by inhibiting the TLR4/ nuclear factor kappa B (NF-κB) signaling pathway. This study helps to further understand the function of tmTNF-α reverse signaling and offers new therapeutic possibilities for sepsis and other inflammatory disease conditions. | ||
| کلیدواژه‌ها | ||
| LPS/TLR4 signaling pathway؛ MCPIP1؛ Reverse signaling؛ SIRT1؛ Transmembrane TNF-α | ||
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آمار تعداد مشاهده مقاله: 506 تعداد دریافت فایل اصل مقاله: 314 |
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