High-density lipoprotein prevents SAA-induced production of TNF-α in THP-1 monocytic cells and peripheral blood mononuclear cells

Memórias do Instituto Oswaldo Cruz

Andressa Grecco Franco¹  Silvana Sandri¹  Ana Campa¹ 

[1] ,Universidade de São Paulo Faculdade de Ciências Farmacêuticas Departamento de Análises Clínicas e ToxicológicasSão Paulo SP ,Brasil

关键词: human serum;    lipoprotein-deficient serum;    peripheral blood mononuclear cells;    proinflammatory cytokines;    serum amyloid A;    THP-1 monocytic lineage;   

DOI  :  10.1590/S0074-02762011000800014

来源: SciELO

【 摘 要 】

In this study, we evaluated whether human serum and lipoproteins, especially high-density lipoprotein (HDL), affected serum amyloid A (SAA)-induced cytokine release. We verified the effects of SAA on THP-1 cells in serum-free medium compared to medium containing human serum or lipoprotein-deficient serum. SAA-induced tumour necrosis factor-alpha (TNF-α) production was higher in the medium containing lipoprotein-deficient serum than in the medium containing normal human serum. The addition of HDL inhibited the SAA-induced TNF-α release in a dose-dependent manner. This inhibitory effect was specific for HDL and was not affected by low-density lipoprotein or very low-density lipoprotein. In human peripheral blood mononuclear cells, the inhibitory effect of HDL on TNF-α production induced by SAA was less pronounced. However, this effect was significant when HDL was added to lipoprotein-deficient medium. In addition, a similar inhibitory effect was observed for interleukin-1 beta release. These findings confirm the important role of HDL and support our previous hypothesis that HDL inhibits the effects of SAA during SAA transport in the bloodstream. Moreover, the HDL-induced reduction in the proinflammatory activity of SAA emphasizes the involvement of SAA in diseases, such as atherosclerosis, that are characterized by low levels of HDL.

【 授权许可】

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