title: Roxithromycin downregulates production of CTACK/CCL27 and MIP-3α/CCL20 from epidermal keratinocytes.
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.
authors.affiliation: Department of Dermatology, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, Japan.
authors.forename: Masaru
authors.initials: M
authors.lastname: Karakawa
authors.forename: Mayumi
authors.initials: M
authors.lastname: Komine
authors.forename: Kunihiko
authors.initials: K
authors.lastname: Tamaki
authors.forename: Mamitaro
authors.initials: M
authors.lastname: Ohtsuki
mesh_terms: D002460:Cell Line; D054418:Chemokine CCL20 / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D054425:Chemokine CCL27 / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation; D004817:Epidermis / Q000473:pathology; D006801:Humans; D007165:Immunosuppression Therapy; D007249:Inflammation; D015603:Keratinocytes / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D016328:NF-kappa B / Q000037:antagonists & inhibitors*; D015575:Roxithromycin / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology / Q000378:metabolism
chemical_list: D054418:Chemokine CCL20; D054425:Chemokine CCL27; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D015575:Roxithromycin