Human β defensin-1 and -2 expression in human pilosebaceous units: upregulation in acne vulgaris lesions

Chronnell, Catherine M. T. and Ghali, Lucy and Ali, Rozina S. and Quinn, Anthony G. and Holland, Diana B. and Bull, Jonathan J. and Cunliffe, William J. and McKay, Ian A. and Philpott, Michael P. and Müller-Röver, Sven (2001) Human β defensin-1 and -2 expression in human pilosebaceous units: upregulation in acne vulgaris lesions. Journal of Investigative Dermatology, 117 (5). pp. 1120-1125. ISSN 0022-202X

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Official URL: http://www.nature.com/jid/journal/v117/n5/full/560...

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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 β defensin-1 and human β 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 β -defensin expression in acne vulgaris lesions compared to controls suggests that β -defensins may be involved in the pathogenesis of acne vulgaris.

Item Type:Article
Additional Information:

PubMed PMID: 11710922. CITED 83

Research Areas:School of Science and Technology > Natural Sciences
Citations on ISI Web of Science:46
ID Code:2537
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Deposited On:22 Jun 2009 08:11
Last Modified:03 Feb 2014 06:58

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