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Updated: Feb 12, 2026

Saturated Fatty Acids Induce Ceramide-associated Macrophage Cell Death
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Stearic Acid Induces CD11c Expression in Proinflammatory Macrophages via Epidermal Fatty Acid Binding Protein

Jun Zeng1,2, Yuwen Zhang1, Jiaqing Hao1

  • 1Department of Microbiology and Immunology, University of Louisville, Louisville, KY 40202.

Journal of Immunology (Baltimore, Md. : 1950)
|April 8, 2018
PubMed

Insights

Dietary saturated fatty acids promote obesity-related inflammation by driving the differentiation of CD11c+ macrophages. This process involves epidermal fatty acid-binding protein (E-FABP) and the retinoid acid receptor.

Area of Science:

  • Immunology
  • Metabolic Disorders
  • Cell Biology

Background:

  • Obesity is linked to increased free fatty acids (FAs) and pro-inflammatory CD11c+ macrophages.
  • The precise role of FAs in CD11c+ macrophage differentiation and function is not fully understood.

Purpose of the Study:

  • To investigate how free fatty acids influence the differentiation and pro-inflammatory functions of CD11c+ macrophages.
  • To elucidate the molecular mechanisms underlying saturated FA-induced macrophage activation in obesity.

Main Methods:

  • Monocyte culture and differentiation assays.
  • Analysis of CD11c expression and nuclear retinoid acid receptor activation.
  • In vitro and in vivo studies using epidermal fatty acid-binding protein (E-FABP) depletion.
  • Murine models of high-saturated-fat diet-induced skin inflammation.

Main Results:

  • Dietary saturated FAs, specifically stearic acid (SA), promote CD11c+ macrophage differentiation and function.
  • SA induces CD11c expression via nuclear retinoid acid receptor activation.
  • Cytosolic E-FABP is essential for mediating SA-induced CD11c upregulation and preventing skin lesions in obese mice.

Conclusions:

  • Saturated FAs, particularly SA, drive obesity-associated inflammation by promoting E-FABP/retinoid acid receptor-mediated differentiation of CD11c+ macrophages.
  • E-FABP plays a critical role in mediating the pro-inflammatory effects of saturated FAs on macrophages.
  • Targeting the E-FABP pathway may offer a therapeutic strategy for obesity-related inflammation.

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