Roxithromycin downregulates production of CTACK/CCL27 and MIP-3α/CCL20 from epidermal keratinocytes

被引：5

作者：

Karakawa, Masaru ^{[1
,2
]}

Komine, Mayumi ^{[1
,2
]}

Tamaki, Kunihiko ^{[2
]}

Ohtsuki, Mamitaro ^{[1
]}

机构：

[1] Jichi Med Univ, Dept Dermatol, Shimotsuke, Tochigi 3290498, Japan

[2] Univ Tokyo, Dept Dermatol, Bunkyo Ku, Tokyo, Japan

来源：

ARCHIVES OF DERMATOLOGICAL RESEARCH | 2010年 / 302卷 / 10期

关键词：

Roxithromycin; Keratinocytes; CTACK/CCL27; MIP-3; alpha/CCL20; NF kappa B; NECROSIS-FACTOR-ALPHA; CHEMOKINE RECEPTOR EXPRESSION; T-CELLS; CCL20; EXPRESSION; KAPPA-B; PSORIASIS; SKIN; PENETRATION; LYMPHOCYTES; INFLIXIMAB;

D O I：

10.1007/s00403-010-1068-x

中图分类号：

R75 [皮肤病学与性病学];

学科分类号：

100206 ;

摘要：

Cutaneous T cell-attracting chemokine (CTACK)/CCL27 and macrophage inflammatory protein (MIP)-3 alpha/CCL20 are the major inflammatory chemokines involved in skin inflammation. The present study showed that roxithromycin (RXM) suppressed the TNF alpha-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 TNF alpha was suppressed by the addition of inhibitors of nuclear factor kappa B (NF kappa B). RXM suppressed NF kappa B activity induced by TNF alpha, RXM, by regulating CCL27 and CCL20, may contribute to the modulation of inflammation.

引用

页码：763 / 767

页数：5

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