title: [Anti-inflammatory effects of apoprotein AI are mediated via modulating macrophage polarity].
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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) .
  
  
  CONCLUSIONS
  ApoAI enhances the switch of inflammatory macrophages to anti-inflammatory macrophages possibly through inhibiting TLR4-MyD88-IRF5 pathway.
authors.affiliation: Department of Cardiology, Affiliated Hospital of Guilin Medical College, Guilin 541001, China. Email: drquanzhongli@163.com.
authors.forename: Quanzhong
authors.initials: Q
authors.lastname: Li
authors.affiliation: Department of Cardiology, Affiliated Hospital of Guilin Medical College, Guilin 541001, China.
authors.forename: Zhenli
authors.initials: Z
authors.lastname: Zhai
authors.affiliation: Department of Cardiology, Affiliated Hospital of Guilin Medical College, Guilin 541001, China.
authors.forename: Weihong
authors.initials: W
authors.lastname: Ma
authors.affiliation: Department of Cardiology, Affiliated Hospital of Guilin Medical College, Guilin 541001, China.
authors.forename: Zongjie
authors.initials: Z
authors.lastname: Qian
mesh_terms: D000818:Animals; D016632:Apolipoprotein A-I / Q000494:pharmacology*; D002460:Cell Line; D005260:Female; D050835:Interferon Regulatory Factors / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D018664:Interleukin-12 / Q000378:metabolism; D037181:Lectins, C-Type / Q000378:metabolism; D008264:Macrophages / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D000090323:Mannose Receptor; D037241:Mannose-Binding Lectins / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D053594:Myeloid Differentiation Factor 88 / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000378:metabolism; D017452:Receptors, IgG / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000378:metabolism
chemical_list: D016632:Apolipoprotein A-I; D050835:Interferon Regulatory Factors; C498178:Irf5 protein, mouse; D037181:Lectins, C-Type; D000090323:Mannose Receptor; D037241:Mannose-Binding Lectins; C507780:Myd88 protein, mouse; D053594:Myeloid Differentiation Factor 88; D011956:Receptors, Cell Surface; D017452:Receptors, IgG; C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4; D016753:Interleukin-10; D018664:Interleukin-12