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

Masaru Karakawa1, Mayumi Komine, Kunihiko Tamaki

  • 1Department of Dermatology, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, Japan.

Archives of Dermatological Research
|July 14, 2010
PubMed

Insights

Roxithromycin (RXM) reduces skin inflammation by suppressing key inflammatory chemokines CCL27 and CCL20. This antibiotic inhibits TNFα-induced chemokine production and NFκB activity, suggesting a role in modulating inflammatory responses.

Area of Science:

  • Dermatology
  • Immunology
  • Pharmacology

Background:

  • Cutaneous T cell-attracting chemokine (CTACK)/CCL27 and macrophage inflammatory protein (MIP)-3α/CCL20 are critical inflammatory mediators in skin conditions.
  • Tumor necrosis factor-alpha (TNFα) plays a significant role in initiating and exacerbating skin inflammation.

Purpose of the Study:

  • To investigate the effect of roxithromycin (RXM) on the production of CCL27 and CCL20 in keratinocytes stimulated with TNFα.
  • To elucidate the underlying mechanism of RXM's action, particularly its impact on nuclear factor kappa B (NFκB) signaling.

Main Methods:

  • HaCaT keratinocytes and normal human keratinocytes (NHKs) were treated with TNFα to induce chemokine production.
  • The effect of varying concentrations of roxithromycin (RXM) on CCL27 and CCL20 levels was assessed.
  • Inhibitors of nuclear factor kappa B (NFκB) and assessment of NFκB activity were used to explore the signaling pathway.

Main Results:

  • Roxithromycin (RXM) significantly suppressed TNFα-induced production of both CCL27 and CCL20 in a dose-dependent manner.
  • The suppression of TNFα-induced CCL20 production by RXM was associated with the inhibition of NFκB activity.
  • RXM demonstrated an inhibitory effect on TNFα-induced NFκB activation in keratinocytes.

Conclusions:

  • Roxithromycin (RXM) effectively modulates key inflammatory chemokines (CCL27 and CCL20) involved in skin inflammation.
  • RXM's anti-inflammatory properties may be mediated through the regulation of the NFκB signaling pathway.
  • These findings suggest RXM has potential therapeutic applications in managing inflammatory skin diseases.

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