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To investigate whether palmitic acid can be responsible for the induction of inflammatory processes, HaCaT keratinocytes were treated with palmitic acid at pathophysiologically relevant concentrations. Secretion levels of interleukin-6 (IL-6), tumor necrosis factor-  α   (TNF-  α  ), interleukin-1  β   (IL-1  β  ), NF-  κ  B nuclear translocation, NF-  κ  B activation, Stat3 phosphorylation, and peroxisome proliferator-activated receptor alpha (PPAR  α  ) mRNA and protein levels, as well as the cell proliferation ability were measured at the end of the treatment and after 24 hours of recovery. Pyrrolidine dithiocarbamate (PDTC, a selective chemical inhibitor of NF-  κ  B) and goat anti-human IL-6 polyclonal neutralizing antibody were used to inhibit NF-  κ  B activation and IL-6 production, respectively. Our results showed that palmitic acid induced an upregulation of IL-6, TNF-  α  , IL-1  β   secretions, accompanied by NF-  κ  B nuclear translocation and activation. Moreover, the effect of palmitic acid was accompanied by PPAR  α   activation and Stat3 phosphorylation. Palmitic acid-induced IL-6, TNF-  α  , IL-1  β   productions were attenuated by NF-  κ  B inhibitor PDTC. Palmitic acid was administered in amounts able to elicit significant hyperproliferation and can be attenuated by IL-6 blockage. These data demonstrate for the first time that palmitic acid can stimulate IL-6, TNF-  α  , IL-1  β   productions in HaCaT keratinocytes and cell proliferation, thereby potentially contributing to acne inflammation and pilosebaceous duct hyperkeratinization.

mediators of inflammation

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Palmitic Acid Induces Production of Proinflammatory Cytokines Interleukin-6, Interleukin-1β, and Tumor Necrosis Factor-αvia a NF-