LPS induces interleukin-6 and interleukin-8 but not tumor necrosis factor-alpha in human adipocytes

Cytokine. 2008 Jan;41(1):29-37. doi: 10.1016/j.cyto.2007.10.008. Epub 2007 Dec 3.

Abstract

Adipose tissue-derived cytokines are presumably involved in obesity-associated pathologies including type 2 diabetes and atherosclerosis. Here we studied the lipopolysaccharide (LPS)-induced expression dynamics of tumor necrosis factor-alpha (TNFalpha), interleukin-6 (IL-6), IL-8 and IL-10 in human adipose tissue biopsies, in preadipocyte-derived adipocytes, and in mesenchymal stem cell (MSC)-derived adipocytes. TNFalpha, IL-6, IL-8 and IL-10 secretions by adipose tissue explants were increased 5.5-, 19.5-, 3.5- and 12.5-fold, respectively, by LPS (1 microg/mL) administration. Concordantly, IL-6 and IL-8 release was dose-dependently induced in MSC-derived adipocytes by LPS (>10 pg/mL). In contrast, TNFalpha and IL-10 remained undetectable even at the highest LPS dose (1 microg/mL) after 24h. In MSC- and preadipocyte-derived adipocytes, respectively, exposure to LPS evoked a weak and transient induction of TNFalpha mRNA whereas induction of IL-6 and IL-8 mRNA were pronounced and sustained for at least 24h. Basal glucose uptake, lipolysis and IL-6 mRNA were induced by exogenous TNFalpha (10 ng/mL) but not by IL-6 (10 ng/mL), IL-8 (100 ng/mL) and IL-10 (20 ng/mL). In this adipocyte model TNFalpha induces well known metabolic effects, but together with previous reports these data suggest that inflammation-induced TNFalpha may derive from non-adipocyte sources in adipose tissue, likely to be macrophages.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipocytes / metabolism*
  • Adipocytes / pathology
  • Atherosclerosis / metabolism
  • Atherosclerosis / pathology
  • Biopsy
  • Cells, Cultured
  • Diabetes Mellitus, Type 2 / metabolism
  • Diabetes Mellitus, Type 2 / pathology
  • Dose-Response Relationship, Drug
  • Gene Expression Regulation / drug effects*
  • Glucose / metabolism
  • Humans
  • Interleukin-10 / biosynthesis
  • Interleukin-6 / biosynthesis*
  • Interleukin-6 / pharmacology
  • Interleukin-8 / biosynthesis*
  • Interleukin-8 / pharmacology
  • Lipolysis / drug effects
  • Lipopolysaccharides / pharmacology*
  • Mesenchymal Stem Cells / metabolism
  • Mesenchymal Stem Cells / pathology
  • Obesity / metabolism
  • Obesity / pathology
  • RNA, Messenger / biosynthesis
  • Time Factors
  • Tumor Necrosis Factor-alpha / biosynthesis*
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • CXCL8 protein, human
  • IL10 protein, human
  • IL6 protein, human
  • Interleukin-6
  • Interleukin-8
  • Lipopolysaccharides
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Interleukin-10
  • Glucose