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Palmitic acid induces production of proinflammatory cytokines interleukin-6, interleukin-1?, and tumor necrosis factor-? via a NF-?B-dependent mechanism in HaCaT keratinocytes.

ABSTRACT: 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- ? (TNF- ?), interleukin-1 ? (IL-1 ?), NF- ? B nuclear translocation, NF- ? B activation, Stat3 phosphorylation, and peroxisome proliferator-activated receptor alpha (PPAR ?) 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- ? B) and goat anti-human IL-6 polyclonal neutralizing antibody were used to inhibit NF- ? B activation and IL-6 production, respectively. Our results showed that palmitic acid induced an upregulation of IL-6, TNF- ? , IL-1 ? secretions, accompanied by NF- ? B nuclear translocation and activation. Moreover, the effect of palmitic acid was accompanied by PPAR ? activation and Stat3 phosphorylation. Palmitic acid-induced IL-6, TNF- ? , IL-1 ? productions were attenuated by NF- ? 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- ? , IL-1 ? productions in HaCaT keratinocytes and cell proliferation, thereby potentially contributing to acne inflammation and pilosebaceous duct hyperkeratinization.

SUBMITTER: Zhou BR

PROVIDER: S-EPMC3774064 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

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Palmitic acid induces production of proinflammatory cytokines interleukin-6, interleukin-1β, and tumor necrosis factor-α via a NF-κB-dependent mechanism in HaCaT keratinocytes.

Zhou Bing-rong BR Zhang Jia-an JA Zhang Qian Q Permatasari Felicia F Xu Yang Y Wu Di D Yin Zhi-qiang ZQ Luo Dan D

Mediators of inflammation 20130829

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 ...[more]

PMID: 24078775

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Project description:Interleukin-1? (IL-1?) and tumor necrosis factor ? (TNF?) stimulate chondrocyte matrix catabolic responses, thereby compromising cartilage homeostasis in osteoarthritis (OA). AMP-activated protein kinase (AMPK), which regulates energy homeostasis and cellular metabolism, also exerts antiinflammatory effects in multiple tissues. This study was undertaken to test the hypothesis that AMPK activity limits chondrocyte matrix catabolic responses to IL-1? and TNF?.Expression of AMPK subunits was examined, and AMPK? activity was ascertained by the phosphorylation status of AMPK? Thr(172) in human knee articular chondrocytes and cartilage by Western blotting and immunohistochemistry, respectively. Procatabolic responses to IL-1? and TNF?, such as release of glycosaminoglycan, nitric oxide, and matrix metalloproteinases 3 and 13 were determined by dimethylmethylene blue assay, Griess reaction, and Western blotting, respectively, in cartilage explants and chondrocytes with and without knockdown of AMPK? by small interfering RNA.Normal human knee articular chondrocytes expressed AMPK?1, ?2, ?1, ?2, and ?1 subunits. AMPK activity was constitutively present in normal articular chondrocytes and cartilage, but decreased in OA articular chondrocytes and cartilage and in normal chondrocytes treated with IL-1? and TNF?. Knockdown of AMPK? resulted in enhanced catabolic responses to IL-1? and TNF? in chondrocytes. Moreover, AMPK activators suppressed cartilage/chondrocyte procatabolic responses to IL-1? and TNF? and the capacity of TNF? and CXCL8 (IL-8) to induce type X collagen expression.Our findings indicate that AMPK activity is reduced in OA cartilage and in chondrocytes following treatment with IL-1? or TNF?. AMPK activators attenuate dephosphorylation of AMPK? and procatabolic responses in chondrocytes induced by these cytokines. These observations suggest that maintenance of AMPK activity supports cartilage homeostasis by protecting cartilage matrix from inflammation-induced degradation.

Dataset Information

Palmitic acid induces production of proinflammatory cytokines interleukin-6, interleukin-1?, and tumor necrosis factor-? via a NF-?B-dependent mechanism in HaCaT keratinocytes.

Publications

Palmitic acid induces production of proinflammatory cytokines interleukin-6, interleukin-1β, and tumor necrosis factor-α via a NF-κB-dependent mechanism in HaCaT keratinocytes.

Similar Datasets

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