1. Centre for Cutaneous Research, St. Bartholomew's and the Royal London School of Medicine and Dentistry, Queen Mary and Westfield College, London, U.K.
2. ^*St. Andrews Centre for Plastic Surgery and Burns, Broomfield Hospital, Chelmsford, Essex, U.K.
3. ^†Department of Dermatology, The General Infirmary at Leeds, Leeds, U.K.

Correspondence: Dr Sven Müller-Röver, Department of Dermatology, Universitäts-Krankenhaus Eppendorf, Universität Hamburg, Martinistr. 52, D-20246 Hamburg, Germany. Email: mueller-roever@web.de

Received 14 August 2001; Revised 7 August 2001; Accepted 23 August 2001.

Abstract

A rich residential microflora is harboured by the distal outer root sheath of the hair follicle and the hair canal – normally without causing skin diseases. Although the basic mechanisms involved in the development of inflammation during acne vulgaris remain unclear, microbial agents might play an important role in this process. In this study we have analyzed by in situ hybridization and immunohistochemistry the expression patterns of two antimicrobial peptides, human defensin-1 and human defensin-2, in healthy human hair follicles as well as in perilesional and intralesional skin of acne vulgaris lesions such as comedones, papules, and pustules. Strong defensin-1 and defensin-2 immunoreactivity was found in all suprabasal layers of the epidermis, the distal outer root sheath of the hair follicle, and the pilosebaceous duct. Marked defensin-1 and defensin-2 immunoreactivity was also found in the sebaceous gland and in the basal layer of the central outer root sheath including the bulge region. The majority of acne biopsies displayed a marked upregulation of defensin-2 immunoreactivity in the lesional and perilesional epithelium – in particular in pustules – and a less marked upregulation of defensin-1 immunoreactivity. The upregulation of -defensin expression in acne vulgaris lesions compared to controls suggests that -defensins may be involved in the pathogenesis of acne vulgaris.