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
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-1β (IL-1β),...
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| Format: | Article |
| Language: | English |
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Wiley
2013-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2013/530429 |
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| author | Bing-rong Zhou Jia-an Zhang Qian Zhang Felicia Permatasari Yang Xu Di Wu Zhi-qiang Yin Dan Luo |
| author_facet | Bing-rong Zhou Jia-an Zhang Qian Zhang Felicia Permatasari Yang Xu Di Wu Zhi-qiang Yin Dan Luo |
| author_sort | Bing-rong Zhou |
| collection | DOAJ |
| description | 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-1β (IL-1β), NF-κB nuclear translocation, NF-κB activation, Stat3 phosphorylation, and peroxisome proliferator-activated receptor alpha (PPARα) 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-κB) and goat anti-human IL-6 polyclonal neutralizing antibody were used to inhibit NF-κB activation and IL-6 production, respectively. Our results showed that palmitic acid induced an upregulation of IL-6, TNF-α, IL-1β secretions, accompanied by NF-κB nuclear translocation and activation. Moreover, the effect of palmitic acid was accompanied by PPARα activation and Stat3 phosphorylation. Palmitic acid-induced IL-6, TNF-α, IL-1β productions were attenuated by NF-κB 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-1β productions in HaCaT keratinocytes and cell proliferation, thereby potentially contributing to acne inflammation and pilosebaceous duct hyperkeratinization. |
| format | Article |
| id | doaj-art-b7cc5199b7cc426295df7ac63a3620b0 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-b7cc5199b7cc426295df7ac63a3620b02025-02-03T05:45:18ZengWileyMediators of Inflammation0962-93511466-18612013-01-01201310.1155/2013/530429530429Palmitic Acid Induces Production of Proinflammatory Cytokines Interleukin-6, Interleukin-1β, and Tumor Necrosis Factor-α via a NF-κB-Dependent Mechanism in HaCaT KeratinocytesBing-rong Zhou0Jia-an Zhang1Qian Zhang2Felicia Permatasari3Yang Xu4Di Wu5Zhi-qiang Yin6Dan Luo7Department of Dermatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, ChinaDepartment of Dermatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, ChinaDepartment of Dermatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, ChinaDepartment of Dermatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, ChinaDepartment of Dermatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, ChinaDepartment of Dermatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, ChinaDepartment of Dermatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, ChinaDepartment of Dermatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, ChinaTo 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-1β (IL-1β), NF-κB nuclear translocation, NF-κB activation, Stat3 phosphorylation, and peroxisome proliferator-activated receptor alpha (PPARα) 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-κB) and goat anti-human IL-6 polyclonal neutralizing antibody were used to inhibit NF-κB activation and IL-6 production, respectively. Our results showed that palmitic acid induced an upregulation of IL-6, TNF-α, IL-1β secretions, accompanied by NF-κB nuclear translocation and activation. Moreover, the effect of palmitic acid was accompanied by PPARα activation and Stat3 phosphorylation. Palmitic acid-induced IL-6, TNF-α, IL-1β productions were attenuated by NF-κB 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-1β productions in HaCaT keratinocytes and cell proliferation, thereby potentially contributing to acne inflammation and pilosebaceous duct hyperkeratinization.http://dx.doi.org/10.1155/2013/530429 |
| spellingShingle | Bing-rong Zhou Jia-an Zhang Qian Zhang Felicia Permatasari Yang Xu Di Wu Zhi-qiang Yin Dan Luo 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 Mediators of Inflammation |
| title | 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 |
| title_full | 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 |
| title_fullStr | 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 |
| title_full_unstemmed | 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 |
| title_short | 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 |
| title_sort | 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 |
| url | http://dx.doi.org/10.1155/2013/530429 |
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