title: Quercetin attenuates inflammation in human macrophages and adipocytes exposed to macrophage-conditioned media.
abstract: BACKGROUND
  Obesity is linked to chronic inflammation in white adipose tissue, which is exacerbated by infiltrating macrophages (MΦs). We recently demonstrated that an extract from grape powder (GPE), which is abundant in quercetin (QUE), reduced inflammation in human MΦs and prevented MΦ-mediated inflammation and insulin resistance in human adipocytes. However, we did not know how QUE individually affected these outcomes.
  
  
  OBJECTIVE
  We examined the extent to which QUE prevents inflammation in human MΦs (that is, differentiated U937 cell line) and cross-talk with human adipocytes (that is, primary cultures of newly differentiated human adipocytes).
  
  
  RESULTS
  Treatment of MΦs with QUE attenuated the basal expression of inflammatory genes, such as tumor necrosis factor-α, interleukin (IL)-6, IL-8, IL-1β and interferon-γ inducible protein-10, and cyclooxygenase-2, a marker of prostaglandin production. QUE also attenuated the abundance of phosphorylated c-Jun N-terminal kinase (JNK) and c-Jun, and IκBα degradation in MΦs. Furthermore, conditioned media (CM) obtained from MΦs treated with QUE decreased the capacity of this CM to inflame adipocytes and cause insulin resistance as evidenced by decreased: (1) inflammatory gene expression, (2) phosphorylation of JNK and c-Jun, (3) serine residue 307 phosphorylation of insulin receptor substrate (IRS)-1, 4) protein tyrosine phosphatase-1B gene expression and 5) suppression of insulin-stimulated glucose uptake.
  
  
  CONCLUSIONS
  Taken together, these data suggest that QUE is one of the bioactive components of GPE that prevents inflammation in MΦs and MΦ-mediated insulin resistance in adipocytes.
authors.affiliation: Department of Nutrition, University of North Carolina-Greensboro, Greensboro, NC 27402-6170, USA.
authors.forename: A
authors.initials: A
authors.lastname: Overman
authors.forename: C-C
authors.initials: CC
authors.lastname: Chuang
authors.forename: M
authors.initials: M
authors.lastname: McIntosh
mesh_terms: D017667:Adipocytes / Q000187:drug effects* / Q000276:immunology; D000328:Adult; D000975:Antioxidants / Q000494:pharmacology*; D002450:Cell Communication / Q000187:drug effects; D002454:Cell Differentiation / Q000187:drug effects; D002478:Cells, Cultured; D017077:Culture Media, Conditioned; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000276:immunology; D018836:Inflammation Mediators / Q000494:pharmacology*; D007333:Insulin Resistance / Q000276:immunology; D007378:Interleukins / Q000276:immunology; D008264:Macrophages / Q000187:drug effects* / Q000276:immunology; D008875:Middle Aged; D009765:Obesity / Q000188:drug therapy / Q000276:immunology; D010936:Plant Extracts / Q000494:pharmacology*; D059808:Polyphenols / Q000494:pharmacology; D011794:Quercetin / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000187:drug effects; D027843:Vitis / Q000737:chemistry
chemical_list: D000975:Antioxidants; D017077:Culture Media, Conditioned; D018836:Inflammation Mediators; D007378:Interleukins; D010936:Plant Extracts; D059808:Polyphenols; D014409:Tumor Necrosis Factor-alpha; D011794:Quercetin