Palmitic acid induces IP-10 expression in human macrophages via NF-κB activation

Phyllis S. Laine, Eric A. Schwartz, Yingjie Wang, Wei Yang Zhang, Sheetal K. Karnik, Nicolas Musi, Peter D. Reaven

Research output: Contribution to journalArticlepeer-review

86 Scopus citations


It is now recognized that cross-talk between adipocytes and adipose tissue stromal cells such as macrophages contributes to local and systemic inflammation. One factor from adipocytes that may participate in this interaction and that is frequently elevated in inflammatory conditions such as obesity, insulin resistance, and type 2 diabetes is free fatty acids (FFA). To investigate the potential for FFA to enhance macrophage inflammation, we exposed U937 macrophages to physiological levels (150 μM) of FFA. Palmitic acid (PA), the predominant saturated FFA released from adipose tissue, but not unsaturated FFA, induced an ∼6-fold (p < 0.05) increase in IP-10 gene expression (and 2- to 4-fold increases in IL-8, MCP-1, COX-2, and MIG). PA also induced an ∼2-fold increase (p < 0.05) in active NF-κB, and two structurally distinct NF-κB inhibitors effectively blocked PA-induced IP-10 gene expression. Conditioned medium from PA-treated cells increased lymphocyte migration 41% (p < 0.05) which was significantly reduced by IP-10-neutralizing antibody. These results suggest that elevated concentrations of PA commonly present in obese and insulin resistant individuals can increase NF-κB-mediated expression of IP-10 in macrophages. These events in turn may lead to an increasing feed-forward loop of chronic inflammation.

Original languageEnglish (US)
Pages (from-to)150-155
Number of pages6
JournalBiochemical and Biophysical Research Communications
Issue number1
StatePublished - Jun 22 2007
Externally publishedYes


  • Free fatty acids
  • IP-10
  • Inflammation
  • Macrophages
  • NF-κB
  • Obesity
  • Palmitic acid

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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