Abstract
Cutaneous T cell-attracting chemokine (CTACK)/CCL27 and macrophage inflammatory protein (MIP)-3α/CCL20 are the major inflammatory chemokines involved in skin inflammation. The present study showed that roxithromycin (RXM) suppressed the TNFα-induced production of CCL27 and CCL20 in HaCaT keratinocytes and normal human keratinocytes (NHKs) in a dose-dependent manner. The production of CCL20 induced by TNFα was suppressed by the addition of inhibitors of nuclear factor kappa B (NFκB). RXM suppressed NFκB activity induced by TNFα. RXM, by regulating CCL27 and CCL20, may contribute to the modulation of inflammation.
MeSH terms
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Cell Line
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Chemokine CCL20 / genetics
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Chemokine CCL20 / immunology
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Chemokine CCL20 / metabolism*
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Chemokine CCL27 / genetics
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Chemokine CCL27 / immunology
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Chemokine CCL27 / metabolism*
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Dose-Response Relationship, Drug
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Down-Regulation
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Epidermis / pathology
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Humans
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Immunosuppression Therapy
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Inflammation
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Keratinocytes / drug effects*
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Keratinocytes / immunology
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Keratinocytes / metabolism
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Keratinocytes / pathology
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NF-kappa B / antagonists & inhibitors*
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Roxithromycin / pharmacology*
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Tumor Necrosis Factor-alpha / immunology
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Tumor Necrosis Factor-alpha / metabolism
Substances
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Chemokine CCL20
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Chemokine CCL27
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NF-kappa B
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Tumor Necrosis Factor-alpha
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Roxithromycin