Severe skin inflammation and filaggrin mutation similarly alter the skin barrier in patients with atopic dermatitis

Mócsai, Gábor; Gáspár, Krisztián; Nagy, Gábor; Irinyi, Beatrix; Kapitány, Anikó; Bı́ró, Tamás; Gyimesi, Edit; Töth, Beáta; Maródi, László; Szegedi, Andrea

doi:10.1111/bjd.12743

Cited by 42 publications

(44 citation statements)

References 41 publications

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“…Th2 cytokines can down-regulate filaggrin protein expression (3) and skin barrier impairment in AD patients with severe skin inflammation seems similar in patients with and without FLG mutations and correlated with the SCORAD. (4) As only patients with severe AD were included in our study (1) , we expect that at initiation of the study levels of skin barrier impairment and inflammation were comparable in the FMG and non-FMG, which is supported by similar mean SCORAD in both groups. When decreasing inflammation by immunosuppressive treatment, downregulation of FLG expression by the inflammatory infiltrate will be abrogated, therefore allowing skin barrier restoration and likely establishment of normal filaggrin protein levels in the non-FMG.…”

Section: Accepted Articlementioning

confidence: 80%

Patients with atopic dermatitis with filaggrin loss-of-function mutations show good but lower responses to immunosuppressive treatment

et al. 2017

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Patients with atopic dermatitis with filaggrin loss-of-function mutations show good but lower responses to immunosuppressive treatment General rightsCopyright and moral rights for the publications made accessible in Discovery Research Portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights.• Users may download and print one copy of any publication from Discovery Research Portal for the purpose of private study or research.• You may not further distribute the material or use it for any profit-making activity or commercial gain.• You may freely distribute the URL identifying the publication in the public portal. Take down policyIf you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim. Accepted ArticleThis article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1111/bjd.15191 This article is protected by copyright. All rights reserved.

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Section: Accepted Articlementioning

confidence: 80%

Patients with atopic dermatitis with filaggrin loss-of-function mutations show good but lower responses to immunosuppressive treatment

et al. 2017

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“…The lack of difference between AD patients with or without FLG variants may be related to the fact that inflammation can downregulate filaggrin levels in the skin. A study of children and adults with AD found that skin barrier was similarly worse in severe AD patients with or without FLG variants compared to mild AD and/or healthy controls, particularly increased TEWL, decreased filaggrin immunostaining, and increased serum levels of TSLP [64].…”

Section: Irritants and Pruritogensmentioning

confidence: 99%

Environmental risk factors and their role in the management of atopic dermatitis

Kantor

Silverberg

2016

Expert Review of Clinical Immunology

240

225

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Introduction-The etiology of atopic dermatitis (AD) is multifactorial with interaction between genetics, immune and environmental factors.Areas covered-We review the role of prenatal exposures, irritants and pruritogens, pathogens, climate factors, including temperature, humidity, ultraviolet radiation, outdoor and indoor air pollutants, tobacco smoke exposure, water hardness, urban vs. rural living, diet, breastfeeding, probiotics and prebiotics on AD.Expert commentary-The increased global prevalence of AD cannot be attributed to genetics alone, suggesting that evolving environmental exposures may trigger and/or flare disease in predisposed individuals. There is a complex interplay between different environmental factors, including individual use of personal care products and exposure to climate, pollution, food and other exogenous factors. Understanding these complex risk factors is crucial to developing targeted interventions to prevent the disease in millions. Moreover, patients require counseling on optimal regimens for minimization of exposure to irritants and pruritogens and other harmful exposures.

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“…No TSLP protein secretion by NHEKs could be detected (not shown). It has previously been found in AD skin that barrier damage can also lead to TSLP production by KCs (Mocsai et al, 2014); therefore, transepidermal water loss and skin pH, representing barrier functions, were measured on SGP and SGR skin regions. No differences were detected, indicating that barrier damage is most probably not the cause of distinct TSLP production in SGR and SGP skin (not shown).…”

Section: Linoleic Acid Induces Tslp Expression In Keratinocytesmentioning

confidence: 99%

Sebaceous Gland-Rich Skin Is Characterized by TSLP Expression and Distinct Immune Surveillance Which Is Disturbed in Rosacea

Dajnoki

Béke

Kapitány

et al. 2017

Journal of Investigative Dermatology

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The microbial community exhibits remarkable diversity on topographically distinct skin regions, which may be accompanied by differences in skin immune characteristics. Our aim was to compare the immune milieu of healthy sebaceous gland rich (SGR) and sebaceous gland poor (SGP) skin areas, and to analyze its changes in an inflammatory disease of SGR skin. For this purpose, immunohistochemical, immunocytochemical and quantitative real-time PCR analyses of thymic stromal lymphopoietin (TSLP) and other cytokines, phenotypic immune cell markers and transcription factors were carried out in samples from SGP, SGR skin and from papulopustular rosacea (PPR). TSLP mRNA and protein production was also studied in cultured keratinocytes. In SGR skin, higher TSLP expression, dendritic cell (DC) appearance without prominent activation and T cell presence with interleukin (IL)-17/IL-10 cytokine milieu were detected compared to SGP skin. Linoleic acid, a major sebum component, was found to induce TSLP expression dose-dependently in keratinocytes. In PPR, significantly decreased TSLP level and influx of inflammatory DCs and T cells with IL-17/interferon-γ cytokine milieu were observed. According to our results, SGR skin is characterized by a distinct, non-inflammatory immune surveillance, which may explain the preferred localization of inflammatory skin diseases, and can influence future barrier repair therapeutic concepts.3

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Severe skin inflammation and filaggrin mutation similarly alter the skin barrier in patients with atopic dermatitis

Cited by 42 publications

References 41 publications

Patients with atopic dermatitis with filaggrin loss-of-function mutations show good but lower responses to immunosuppressive treatment

Patients with atopic dermatitis with filaggrin loss-of-function mutations show good but lower responses to immunosuppressive treatment

Environmental risk factors and their role in the management of atopic dermatitis

Sebaceous Gland-Rich Skin Is Characterized by TSLP Expression and Distinct Immune Surveillance Which Is Disturbed in Rosacea

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