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: Masaru Karakawa, Mayumi Komine, Kunihiko Tamaki, Mamitaro Ohtsuki
• Journal: Archives of dermatological research (Arch Dermatol Res) Vol. 302 Issue 10 Pg. 763-7 (Dec 2010) ISSN: 1432-069X [Electronic] Germany
• PMID: 20625754 (Publication Type: Journal Article)

Chemical References

• Chemokine CCL20
• Chemokine CCL27
• NF-kappa B
• Tumor Necrosis Factor-alpha
• Roxithromycin

Topics

• Cell Line
• Chemokine CCL20 (genetics, immunology, metabolism)
• Chemokine CCL27 (genetics, immunology, metabolism)
• Dose-Response Relationship, Drug
• Down-Regulation
• Epidermis (pathology)
• Humans
• Immunosuppression Therapy
• Inflammation
• Keratinocytes (drug effects, immunology, metabolism, pathology)
• NF-kappa B (antagonists & inhibitors)
• Roxithromycin (pharmacology)
• Tumor Necrosis Factor-alpha (immunology, metabolism)