1. ¹Institute for Anatomy and Cell Biology, University of Giessen, Giessen, Germany
2. ²Department of Psychosomatic Medicine, University of Giessen, Giessen, Germany
3. ³Department of Dermatology and Andrology, University of Giessen, Giessen, Germany
4. ⁴Division of Reproductive Biology, Department of Obstetrics and Gynecology, Stanford University School of Medicine, Stanford, UK
5. ⁵Department of Dermatology, IZKF Munster and Ludwig Boltzmann Institute for Cell- and Immunobiology of the Skin, University of Munster, Munster, Germany

Correspondence: Dr Rainer Viktor Haberberger, Department for Anatomy and Histology, GPO Box 2100, Flinders-University Adelaide, Adelaide 5001, Australia. E-mail: rainer.haberberger@flinders.edu.au

Received 25 September 2005; Revised 27 June 2006; Accepted 15 August 2006; Published online 28 September 2006.

Abstract

Intermedin (IMD), also called adrenomedullin-2, is a peptide that belongs to the calcitonin/calcitonin gene-related peptide/amylin peptide family. IMD exerts many effects on the cardiovascular system, gastrointestinal tract, and central nervous system. Here, we analyzed the expression of the IMD peptide in human skin of healthy controls, in biopsies from lesional and non-lesional areas of atopic dermatitis (AD) skin, in cultured human keratinocytes, and in the HaCaT keratinocyte cell line at the transcriptional (quantitative reverse transcription-PCR) and translational (immunohistochemistry) level. IMD messenger RNA (mRNA) and protein could be detected in keratinocytes and human skin. Keratinocytes, nerve fibers, periglandular cells, arterial/arteriolar smooth muscle cells, and pericytes of dermal microvessels were intensely IMD-immunoreactive. The IMD mRNA was, compared to healthy skin, significantly reduced in lesional and non-lesional areas of AD skin. This was accompanied by a reduction of IMD immunoreactivity in pericytes of the upper dermis indicating that skin from AD patients is generally affected, and downregulation of IMD in AD skin is not a secondary phenomenon caused by acute inflammation but is a general characteristic of AD skin. These data further point to a role of IMD expressed by pericytes in conferring higher susceptibility of the skin of AD patients to inflammatory stimuli.