Anti-inflammatory effects of apoprotein AI are mediated via modulating macrophage polarity / 中华心血管病杂志

ABSTRACT

<p><b>OBJECTIVE</b>To explore the anti-inflammatory mechanisms of high density lipoprotein (HDL) by observing the effects of apoprotein (apo)AI, a major protein component of HDL, on the inflammatory macrophage cell polarity.</p><p><b>METHODS</b>Cultured mice marrow-derived macrophages were stimulated with lipopolysaccharide and interferon after 10 µg/ml of apoAI were added to the macrophages for 24 hours. The expression of membrane molecules CD16/32, CD206 were detected by fluorescence activated cell sorting (FACS). ELISA was used to detect the secretion of IL-10 and IL-12. Real-time quantitative PCR was used to detect the mRNA expression of TLR4, MyD88 and IRF5.</p><p><b>RESULTS</b>Compared to macrophages stimulated by interferon and lipopolysaccharide but without pretreatment with apoAI, pre-incubation with apoAI significantly downregulated the expression of CD16/32 (91.17% ± 1.99% vs.50.47% ± 1.02%, P < 0.05), IL-12 [(747.27 ± 3.74)pg/ml vs. (73.80 ± 4.56)pg/ml, P < 0.05], upregulated the expression of CD206(0.33% ± 0.12% vs. 3.00% ± 0.36%, P < 0.05), IL -10 expression [(23.56 ± 4.30) pg/ml vs.(32.91 ± 2.47) pg/ml, P < 0.05], and reduced the mRNA expression of TLR4 (1.000 ± 0.025 vs.0.708 ± 0.003, P < 0.05) , MyD88 (1.591 ± 0.005 vs. 1.341 ± 0.005, P < 0.05) , IRF5 (0.954 ± 0.005 vs. 0.463 ± 0.003, P < 0.05) .</p><p><b>CONCLUSION</b>ApoAI enhances the switch of inflammatory macrophages to anti-inflammatory macrophages possibly through inhibiting TLR4-MyD88-IRF5 pathway.</p>