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Published on: December 23, 2010

Inflammation resolved by retinoid X receptor-mediated inactivation of leukotriene signaling pathways

Auinash Kalsotra1, Liping Du, Ying Wang

  • 1University of Texas Health Science Center at Houston, 6431 Fannin St., Medical School Bldg. 6, Room 200, Houston, TX 77030, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|September 22, 2007
PubMed

Insights

Leukotriene hydroxylases (CYP4F) in skin inactivate inflammatory leukotrienes. Therapeutic retinoids boost CYP4F activity, reducing inflammation and restoring skin barrier function.

Area of Science:

  • Biochemistry
  • Dermatology
  • Pharmacology

Background:

  • Leukotrienes contribute to inflammation in various diseases.
  • Mechanisms for leukotriene inactivation in peripheral tissues are poorly understood.
  • Human skin is a common site for inflammatory diseases and drug reactions.

Purpose of the Study:

  • Investigate leukotriene hydroxylases (CYP4F) in human skin.
  • Determine the role of CYP4F in inflammatory skin conditions.
  • Elucidate the anti-inflammatory effects of therapeutic retinoids on CYP4F.

Main Methods:

  • Studied CYP4F gene products in human skin.
  • Analyzed CYP4F expression in epidermal keratinocytes.
  • Examined regulation of CYP4F by differentiation factors and retinoids in vitro.
  • Assessed CYP4F expression in skin with hyperproliferative dermatoses and after retinoid therapy.

Main Results:

  • Human epidermis expresses multiple CYP4F enzymes, notably CYP4F3A, a key leukotriene B4 hydroxylase.
  • CYP4F expression is upregulated in hyperproliferative dermatoses and by retinoid therapy.
  • Retinoids increase leukotriene B4 hydroxylation (inactivation) via retinoid X receptor interactions with CYP4F promoters.

Conclusions:

  • Enhanced CYP4F-mediated leukotriene inactivation is an innate anti-inflammatory mechanism in skin.
  • Therapeutic retinoids possess anti-inflammatory properties by upregulating skin CYP4F activity.
  • This highlights a novel pathway for retinoid action in inflammatory skin diseases.

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