Involvement of the corticotropin-releasing hormone system in the pathogenesis of acne vulgaris.
Br J Dermatol. 2009 Feb;160(2):345-52. Epub 2008 Dec 10.
Ganceviciene R, Graziene V, Fimmel S, Zouboulis CC.
Ganceviciene R, Graziene V, Fimmel S, Zouboulis CC.
Centre of Dermatovenereology, Vilnius University Hospital, Santariskiu Klinikos, Vilnius, Lithuania.
Comment in:
Br J Dermatol. 2009 Feb;160(2):229-32.
BACKGROUND:
The sebaceous gland exhibits an independent peripheral endocrine function and expresses receptors for neuropeptides.
Previous reports have confirmed the presence of a complete corticotropin-releasing hormone (CRH) system in human sebocytes in vitro.
The capability of hypothalamic CRH to induce lipid synthesis, induce steroidogenesis and interact with testosterone and growth hormone implicates a possibility of its involvement in the clinical development of acne.
OBJECTIVES:
The purpose of the study was to detect expression changes of CRH/CRH binding protein (CRHBP)/CRH receptors (CRHRs) in acne-involved skin, especially in the sebaceous glands.
METHODS:
Expression of CRH/CRHBP/CRHRs was analysed by immunohistochemistry in biopsies from facial skin of 33 patients with acne, noninvolved thigh skin of the same patients and normal skin of eight age-matched healthy volunteers.
RESULTS:
Very strong positive reaction for CRH was observed in acne-involved skin in all types of sebaceous gland cells, irrespective of their differentiation stage, whereas in noninvolved and normal skin sebaceous glands exhibited a weaker CRH staining depending upon the differentiation stage of sebocytes.
The strongest reaction for CRHBP (binding protein) in acne-involved sebaceous glands was in differentiating sebocytes.
CRHR-1 and CRHR-2 exhibited the strongest expression in sweat glands and sebaceous glands, respectively.
CONCLUSIONS:
Expression of the complete CRH system is abundant in acne-involved skin, especially in the sebaceous glands, possibly activating pathways which affect immune and inflammatory processes leading to the development and stress-induced exacerbation of acne.
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=19077080%5Buid%5D
SEE ALSO (pdf file):
Differential Expression of a Cutaneous Corticotropin-
Releasing Hormone System
Copyright © 2005 Elsevier Ltd All rights reserved.
Neuroimmunoendocrine circuitry of the ‘brain-skin connection’
aDepartment of Dermatology, University Hospital Schleswig-Holstein, Campus Lübeck, University of Lübeck, D-23538 Lübeck, Germany
bDepartments of Pharmacology & Experimental Therapeutics, Biochemistry and Internal Medicine, Tufts University School of Medicine, Boston, MA 02111, USA
cBiomedical Research Center, Charité – University Medicine Berlin, D-13353 Berlin, Germany
Available online 2 November 2005.
The skin offers an ideally suited, clinically relevant model for studying the crossroads between peripheral and systemic responses to stress.
A ‘brain–skin connection’ with local neuroimmunoendocrine circuitry underlies the pathogenesis of allergic and inflammatory skin diseases, triggered or aggravated by stress.
In stressed mice, corticotropin-releasing hormone (CRH), nerve growth factor, neurotensin, substance P and mast cells are recruited hierarchically to induce neurogenic skin inflammation, which inhibits hair growth.
The hair follicle is both a target and a source for immunomodulatory stress mediators, and has an equivalent of the hypothalamus–pituitary–adrenal axis.
Thus, the skin and its appendages enable the study of complex neuroimmunoendocrine responses that peripheral tissues launch upon stress exposure, as a basis for identifying new targets for therapeutic stress intervention.
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