Mechanisms for the anti‐inflammatory effects of adiponectin in macrophages

脂联素 肿瘤坏死因子α 脂多糖 细胞因子 医学 内分泌学 脂肪因子 巨噬细胞 内科学 炎症 信号转导 酒精性肝病 受体 细胞生物学 癌症研究 生物 生物化学 体外 胰岛素抵抗 肝硬化 胰岛素
作者
Honglian Huang,Pil‐Hoon Park,Megan R. McMullen,Laura E. Nagy
出处
期刊:Journal of Gastroenterology and Hepatology [Wiley]
卷期号:23 (s1) 被引量:87
标识
DOI:10.1111/j.1440-1746.2007.05284.x
摘要

Abstract Adiponectin is an adipokine with potent anti‐inflammatory properties. The development of alcoholic liver disease is thought to involve increased pro‐inflammatory activity, mediated in part by the activation of hepatic macrophages (Kupffer cells). Chronic ethanol feeding sensitizes hepatic macrophages to activation by lipopolysaccharide (LPS), leading to increased production of reactive oxygen species and tumor necrosis factor‐α (TNF‐α). Adiponectin can normalize Toll‐like receptor‐4 (TLR‐4) mediated signaling in hepatic macrophages after ethanol feeding, likely contributing to the hepatoprotective effect of adiponectin in the progression of alcoholic liver disease. However, the mechanisms by which adiponectin suppress TLR‐4 mediated responses are not well understood. Using the macrophage‐like cell line, RAW264.7, we have investigated the molecular mechanisms by which adiponectin suppresses LPS‐stimulated TNF‐α production. Globular adiponectin (gAcrp)‐mediated desensitization of LPS‐stimulated responses in RAW264.7 macrophages was dependent on the production of the anti‐inflammatory cytokine interleukin (IL)‐10. gAcrp initially increased TNF‐α expression in RAW264.7 macrophages; this TNF‐α then contributed to increased expression of IL‐10. This initial gAcrp‐mediated increase in TNF‐α production by macrophages was mediated via activation of ERK1/2→Egr‐1 and nuclear factor (NF)‐κB‐dependent mechanisms. gAcrp‐stimulated IL‐10 expression was also dependent on the phosphorylation of cAMP response element‐binding protein and the cAMP response element in the IL‐10 promoter. In summary, these studies reveal a complex, integrated response of macrophages to gAcrp. gAcrp initially activated signaling pathways considered to be pro‐inflammatory, with a subsequent increase in the expression of the potent, anti‐inflammatory cytokine, IL‐10. Increased IL‐10 expression was ultimately required for the suppression of TLR4‐mediated signaling by gAcrp.

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