Abnormal Epidermal Barrier Recovery in Uninvolved Skin Supports the Notion of an Epidermal Pathogenesis of Psoriasis

Autor: Peter M. Elias, Mao-Qiang Man, George Man, Li Ye, Chengzhi Lv, Shunpeng Song
Rok vydání: 2014
Předmět:
Zdroj: The Journal of investigative dermatology
The Journal of investigative dermatology, vol 134, iss 11
Ye, L; Lv, C; Man, G; Song, S; Elias, PM; & Man, MQ. (2014). Abnormal epidermal barrier recovery in uninvolved skin supports the notion of an epidermal pathogenesis of psoriasis. Journal of Investigative Dermatology, 134(11), 2843-2846. doi: 10.1038/jid.2014.205. UC San Francisco: Retrieved from: http://www.escholarship.org/uc/item/6np1s4q8
ISSN: 0022-202X
DOI: 10.1038/jid.2014.205
Popis: HHS Public Access Author manuscript Author Manuscript J Invest Dermatol. Author manuscript; available in PMC 2015 May 01. Published in final edited form as: J Invest Dermatol. 2014 November ; 134(11): 2843–2846. doi:10.1038/jid.2014.205. Abnormal Epidermal Barrier Recovery in Uninvolved Skin supports the Notion of an Epidermal Pathogenesis of Psoriasis Li Ye 1 , Chengzhi Lv 1 , George Man 2 , Shunpeng Song 1 , Peter M. Elias 2 , and Mao-Qiang Man 2 1 Dalian Skin Disease Hospital, Liaoning, P.R. China 2 Dermatology Author Manuscript Services, Veterans Affair Medical Center and University of California San Francisco, CA, USA Keywords Psoriasis; Stratum Corneum; Permeability Barrier; Hydration; pH; Transepidermal Water Loss To The Editor Author Manuscript Psoriasis is generally considered to be an immunologically-initiated disorder, which shares certain common susceptibility loci with autoimmune diseases (Zhang, 2012). Yet, both clinical experience (Gottlieb et al.,1990; Griffiths et al., 1995; Volden et al., 2001;) and recent molecular studies (Bergboer et al., 2012; Kim et al., 2011; Mischke et al., 1996; Vermeij et al., 2011) support an emerging concept that psoriasis could be ‘driven’ by a primary defect in epidermal permeability barrier function. Clinicians know well that psoriasis predictably flares during winter months (Park and Youn, 1998; Kwon et al., 2012), when the barrier is under additional stress due to low stratum corneum hydration, which accelerates transepidermal water loss (TEWL) rates (Lin, 2009; Muizzuddin et al., 2013). They also appreciate that sites vulnerable to epidermal trauma, such as the extensors of the extremities and the scalp, are preferentially involved in psoriasis. The Koebner phenomenon offers an additional, eloquent example of how psoriasis can be provoked by external perturbations. Finally, improvement of epidermal permeability barrier function by occlusion alone often alleviates psoriasis (e.g., Friedman, 1987). Author Manuscript Among psoriasis susceptibility genes, PSORS4 is located on chromosome 1q21, within the epidermal differentiation complex, which encodes numerous proteins required for epidermal differentiation and the formation of the cornified envelope (Mischke et al., 1996), a structure that is critical for the permeability barrier (Vermeij et al., 2011). Additionally, deletion of differentiation-related proteins, such as keratin1, whose levels are reduced in psoriasis (Thewes et al., 1991; Bata-Csorgo and Szell, 2012), not only compromises the permeability barrier, but also leads to upregulation of inflammatory genes and altered cytokine production Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:http://www.nature.com/authors/editorial_policies/license.html#terms Address Correspondence To: Mao-Qiang Man, MD, Dermatology Service (190), 4150 Clement Street, San Francisco, CA 94121, USA, Tel: (415)750-2091, Fax: (415)750-2106, mqman@hotmail.com Or Chengzhi Lv, MD, dlpfb@126.com. All authors declare no conflicts of interest
Databáze: OpenAIRE
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