Dexmedetomidine modulates peritoneal macrophage to attenuate lipopolysaccharide-induced inflammation

IF 3.7 4区 医学 Q2 CELL BIOLOGY
Tao Wang , Rui Pan , Jianli Wen , Xinglong Ma
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引用次数: 0

Abstract

Purpose

To investigate how Dexmedetomidine (Dex) modulates the function of peritoneal macrophages (PMs) to reduce lipopolysaccharide (LPS)-induced inflammation.

Methods

The anti-inflammatory effect of Dex on LPS-stimulated PMs was assessed by examining its impact on their proliferation, phagocytosis, and polarization. Proliferation and phagocytic activity were measured using CCK-8 and Neutral Red staining assays, respectively. The levels of inflammatory mediators were quantified using ELISA. Additionally, macrophage polarization was evaluated via ELISA, flow cytometry, and Western blot analysis to identify shifts in macrophage phenotypes.

Results

Dex increased the proliferation and phagocytic capabilities of PMs, thereby mitigating LPS-induced inflammation. It suppressed pro-inflammatory mediators, including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and high mobility group box 1 (HMGB1), while increasing levels of the anti-inflammatory cytokine interleukin-10 (IL-10). Furthermore, Dex promoted M2-type macrophage polarization, characterized by increased expression of IL-10, CD206, Arg-1, and CD11c. This effect was mediated through the JAK1/STAT6 signaling pathway, promoting M2 polarization, which was attenuated when JAK1 and STAT6 expression were downregulated.

Conclusion

Dex reduces LPS-induced inflammation in part by enhancing the proliferation, phagocytosis, and M2 polarization of PMs, with a key role for the JAK1/STAT6 pathway in promoting anti-inflammatory responses during sepsis.
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来源期刊
Cellular immunology
Cellular immunology 生物-免疫学
CiteScore
8.20
自引率
2.30%
发文量
102
审稿时长
30 days
期刊介绍: Cellular Immunology publishes original investigations concerned with the immunological activities of cells in experimental or clinical situations. The scope of the journal encompasses the broad area of in vitro and in vivo studies of cellular immune responses. Purely clinical descriptive studies are not considered. Research Areas include: • Antigen receptor sites • Autoimmunity • Delayed-type hypersensitivity or cellular immunity • Immunologic deficiency states and their reconstitution • Immunologic surveillance and tumor immunity • Immunomodulation • Immunotherapy • Lymphokines and cytokines • Nonantibody immunity • Parasite immunology • Resistance to intracellular microbial and viral infection • Thymus and lymphocyte immunobiology • Transplantation immunology • Tumor immunity.
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