Toll-like receptor 2 activation and comedogenesis: implications for the pathogenesis of acneReportar como inadecuado




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BMC Dermatology

, 13:10

First Online: 06 September 2013Received: 22 March 2013Accepted: 28 August 2013

Abstract

BackgroundAcne is a common disorder of the human pilosebaceous unit, yet the mechanisms underlying hyperkeratinisation and subsequent inflammation comedogenesis remain to be determined, although cutaneous pathogens are implicated. Previously, it was reported that the release of the cytokine interleukin-1α IL-1α by keratinocytes of the sebaceous duct was pivotal in the life cycle of the comedone, mediating both its development and its spontaneous resolution. Toll-like receptors are a family of molecules that recognise pathogen associated molecular patterns PAMPs presented by microorganisms, initiating a signalling cascade terminating in the release of antimicrobial compounds and cytokines.

MethodsWe used ex vivo sebaceous gland and primary monolayer keratinocyte culture, alongside ELISAs, immunohistochemistry, Western blotting and RT-PCR to investigate the contribution of TLR activation to acne pathogenesis.

ResultsWe found TLR2 to be expressed in basal and infundibular keratinocytes, and sebaceous glands, and its activation provoked the release of IL-1α from primary human keratinocytes in vitro. The exposure of microdissected human sebaceous glands to PAMPs specific for TLR2 in vitro resulted in a pattern of IL-1α like cornification after seven days of exposure.

ConclusionsTLR activation and secretion of IL-1α from keratinocytes may be initiating steps in comedogenesis and, therefore, critical to the pathophysiology of acne.

KeywordsAcne vulgaris Toll-like receptors Peptidoglycan Interleukin-1alpha Keratinocytes Electronic supplementary materialThe online version of this article doi:10.1186-1471-5945-13-10 contains supplementary material, which is available to authorized users.

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Autor: Joanne Louise Selway - Tomasz Kurczab - Terence Kealey - Kenneth Langlands

Fuente: https://link.springer.com/







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