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      Rosacea: Epidemiology, pathogenesis, and treatment

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          ABSTRACT

          Rosacea is a chronic relapsing inflammatory skin disease with a high prevalence among adults of Northern European heritage with fair skin. Symptoms present in various combinations and severity, often fluctuating between periods of exacerbation and remission. Based on morphological characteristics, rosacea is generally classified into four major subtypes: erythematotelangiectatic, papulopustular, phymatous, and ocular. Diverse environmental and endogenous factors have been shown to stimulate an augmented innate immune response and neurovascular dysregulation; however, rosacea's exact pathogenesis is still unclear. An evidence-based approach is essential in delineating differences between the many available treatments. Because of the diverse presentations of rosacea, approaches to treatment must be individualized based on the disease severity, quality-of-life implications, comorbidities, trigger factors, and the patient's commitment to therapy.

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          Most cited references101

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          The vanilloid receptor: a molecular gateway to the pain pathway.

          The detection of painful stimuli occurs primarily at the peripheral terminals of specialized sensory neurons called nociceptors. These small-diameter neurons transduce signals of a chemical, mechanical, or thermal nature into action potentials and transmit this information to the central nervous system, ultimately eliciting a perception of pain or discomfort. Little is known about the proteins that detect noxious stimuli, especially those of a physical nature. Here we review recent advances in the molecular characterization of the capsaicin (vanilloid) receptor, an excitatory ion channel expressed by nociceptors, which contributes to the detection and integration of pain-producing chemical and thermal stimuli. The analysis of vanilloid receptor gene knockout mice confirms the involvement of this channel in pain sensation, as well as in hypersensitivity to noxious stimuli following tissue injury. At the same time, these studies demonstrate the existence of redundant mechanisms for the sensation of heat-evoked pain.
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            Intracellular pattern recognition receptors in the host response.

            The innate immune system relies on its capacity to rapidly detect invading pathogenic microbes as foreign and eliminate them. Indeed, Toll-like receptors are a class of membrane receptors that sense extracellular microbes and trigger anti-pathogen signalling cascades. Recently, intracellular microbial sensors have also been identified, including NOD-like receptors and the helicase-domain-containing antiviral proteins RIG-I and MDA5. Some of these cytoplasmic molecules sense microbial, as well as non-microbial, danger signals, but the mechanisms of recognition used by these sensors remain poorly understood. Nonetheless, it is apparent that these proteins are likely to have critical roles in health and disease.
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              Increased serine protease activity and cathelicidin promotes skin inflammation in rosacea.

              Acne rosacea is an inflammatory skin disease that affects 3% of the US population over 30 years of age and is characterized by erythema, papulopustules and telangiectasia. The etiology of this disorder is unknown, although symptoms are exacerbated by factors that trigger innate immune responses, such as the release of cathelicidin antimicrobial peptides. Here we show that individuals with rosacea express abnormally high levels of cathelicidin in their facial skin and that the proteolytically processed forms of cathelicidin peptides found in rosacea are different from those present in normal individuals. These cathelicidin peptides are a result of a post-translational processing abnormality associated with an increase in stratum corneum tryptic enzyme (SCTE) in the epidermis. In mice, injection of the cathelicidin peptides found in rosacea, addition of SCTE, and increasing protease activity by targeted deletion of the serine protease inhibitor gene Spink5 each increases inflammation in mouse skin. The role of cathelicidin in enabling SCTE-mediated inflammation is verified in mice with a targeted deletion of Camp, the gene encoding cathelicidin. These findings confirm the role of cathelicidin in skin inflammatory responses and suggest an explanation for the pathogenesis of rosacea by demonstrating that an exacerbated innate immune response can reproduce elements of this disease.
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                Author and article information

                Journal
                Dermatoendocrinol
                Dermatoendocrinol
                KDER
                kder20
                Dermato-endocrinology
                Taylor & Francis
                1938-1972
                1938-1980
                2017
                4 October 2017
                4 October 2017
                : 9
                : 1
                : e1361574
                Affiliations
                [a ]Department of Dermatology, Medical University of Graz , Graz, Austria
                [b ]Department of Dermatology, Johns Hopkins University School of Medicine , Baltimore, MD, USA
                Author notes
                CONTACT Barbara M. Rainer, MD bm.rainer@ 123456gmail.com Department of Dermatology, Medical University of Graz , Auenbruggerplatz 8, 8036 Graz, Austria

                This paper is part of the special section based on the 3rd ICSGAD conference held in September 2016.

                Article
                1361574
                10.1080/19381980.2017.1361574
                5821167
                29484096
                80ad07fd-f950-49c2-a9de-aa9f0c54b8f8
                © 2018 The Author(s). Published with license by Taylor & Francis

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License ( http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.

                History
                : 1 June 2017
                : 26 July 2017
                Page count
                Figures: 0, Tables: 1, Equations: 0, References: 105, Pages: 10
                Categories
                Review

                Dermatology
                comorbidities,genetics,innate immunity,management,neurovascular dysregulation,prevalence,quality-of-life

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