scholarly journals Role of skin microbiome in epidermal barrier dysfunction and development of atopic dermatitis in high risk infants

2019 ◽  
Vol 16 (1) ◽  
pp. 59-64
Author(s):  
N B Migacheva

Background. Colonization of skin with S. aureus in atopic dermatitis (AD) patients is a widespread phenomenon and a factor complicating the course of the disease. At present, it is not quite clear the role of S. aureus in the development of AD in children at risk. The aim of our study was to discribe the skin microbiome composition in young children at risk, as well as to investigate the role of S. aureus in skin barrier dysfunction and the development of AD. Material and methods. 12months follow-up study of 37 infants at risk has been performed. It included a general clinical examination, a microbiological investigation of skin microbiome (at 1 and 6 months), and investigation of epidermal barrier function by determining the transepidermal water loss (TEWL) at 1, 3, 6 and 12 months. Realization of AD during the observation period was considered as main outcome. Results. The prevalence of S. aureus colonization of infants aged 1 month was 45.9%, at the age of 6 months - 29.7%. Correlation analysis revealed an association between the skin colonization with S. aureus and a decrease of TEWL (p = 0.004), as well as the cumulative incidence of AD (p


Author(s):  
N.B. Migacheva

Обоснование. Нарушение кожного микробиоценоза и колонизация кожи S. aureus при атопическом дерматите (АтД) является широко распространенным феноменом и фактором, осложняющим течение заболевания. В настоящее время не вполне понятно, какую роль играет S. aureus в реализации АтД у детей из группы риска по развитию аллергических заболеваний. Цель. Изучение состава кожного микробиоценоза у детей раннего возраста из группы риска, а также роли S. aureus в дисфункции кожного барьера и реализации АтД. Материалы и методы. Проведен анализ 12-месячного наблюдения за 37 детьми из группы риска по развитию аллергических заболеваний, включающий общеклиническое обследование, проведение микробиологического исследования кожи в возрасте 1 и 6 мес и изучение функции эпидермального барьера путем определения показателя трансэпидермальной потери влаги (ТЭПВ) в возрасте 1 3 6 и 12 мес. В качестве исхода рассматривалось формирование АтД в течение периода наблюдения. Результаты. Частота выявления S. aureus на коже детей в возрасте 1 мес составила 45,9, в возрасте 6 мес - 29,7. Корреляционный анализ выявил ассоциацию между колонизацией кожи S. aureus и снижением показателей ТЭПВ (р0,004), а также частотой развития у них АтД (p0,001). Заключение. Обнаружение S. aureus в кожном микробиоценозе детей из группы риска ассоциировано с дисфункцией эпидермального барьера и является значимым фактором риска реализации у них АтД.Background. Colonization of skin with S. aureus in atopic dermatitis (AD) patients is a widespread phenomenon and a factor complicating the course of the disease. At present, it is not quite clear the role of S. aureus in the development of AD in children at risk. The aim of our study was to discribe the skin microbiome composition in young children at risk, as well as to investigate the role of S. aureus in skin barrier dysfunction and the development of AD. Material and methods. 12months follow-up study of 37 infants at risk has been performed. It included a general clinical examination, a microbiological investigation of skin microbiome (at 1 and 6 months), and investigation of epidermal barrier function by determining the transepidermal water loss (TEWL) at 1, 3, 6 and 12 months. Realization of AD during the observation period was considered as main outcome. Results. The prevalence of S. aureus colonization of infants aged 1 month was 45.9, at the age of 6 months - 29.7. Correlation analysis revealed an association between the skin colonization with S. aureus and a decrease of TEWL (p 0.004), as well as the cumulative incidence of AD (p 0.001). Conclusion. The detection of S. aureus as a part of skin microbiocenosis in AD infants at risk is associated with dysfunction of the epidermal barrier and is a significant risk factor for the AD development.



2014 ◽  
Vol 11 (3) ◽  
pp. 47-52
Author(s):  
A N KHLEBNIKOVA

Epidermal barrier insufficiency results in skin dryness and fissures in different chronic dermatoses. Barrier dysfunction is due either to genetic problems or lipid deficiency or damage of tight junction proteins. Here we discuss various abnormalities of epidermal barrier in eczema and psoriasis which necessitate to prescribe pro- tective and moisturizing agents to restore skin barrier. We give our own practice data of using Bariederm cream and balm in combined therapy of dyshidrotic eczema, plantar eczema and palmoplantar psoriasis.



2021 ◽  
Vol 79 (3) ◽  
pp. 207-216
Author(s):  
Tiago Fernandes Gomes ◽  
Rebeca Calado ◽  
Margarida Gonçalo

Impaired skin barrier is one of the hallmarks of atopic dermatitis (AD), with abnormalities in the cornified envelope, lipid lamellae, tight junctions and cutaneous microbiome. These findings are also present in nonlesional skin of AD individuals, suggesting that epidermal barrier defects may be the initial step towards the development of AD and eventually other atopic diseases (atopic march). It is currently known that pathophysiology of AD involves an interplay between this dysfunctional skin barrier and a predominantly type 2 skewed innate and adaptive immune responses, which further disrupt the skin barrier through type 2 cytokines. In this setting, there is enhanced penetration of environmental and food allergens through a deficient barrier, leading to an increased susceptibility to sensitization. During the sensitization process, thymic stromal lymphopoietin (TSLP) polarizes skin dendritic cells to a T-helper 2 response, and TSLP seems to be a key cytokine in the sensitization of food allergy, allergic asthma and rhinitis. In this review, the authors describe the current knowledge of the pathophysiology of the epidermal barrier, its disruption in AD and how it may be involved in the development of atopic comorbidities and the role of barrier repair therapy on the prevention of the atopic march progression.  



2021 ◽  
Author(s):  
◽  
Karmella Naidoo

<p>Atopic dermatitis (AD) is a highly debilitating disease with significant health impacts worldwide. It is a chronic and relapsing inflammatory skin disease which often poses a life-long burden for the affected individuals. AD has been a difficult disease to treat as it manifests with a wide spectrum of clinical phenotypes and the current clinical management strategies are non-specific. Therefore, it is imperative to identify specific immunological pathways that could be targeted to treat this disease. Previous studies have documented that AD disease progression is precipitated by a combination of skin barrier dysfunction, itch and immune dysregulation that are responsible for AD progression. However, the precise role of effector cells and cytokines have not been fully elucidated. To address this, I established a clinically relevant model of AD, using the vitamin D analogue, MC903. This MC903 model closely resembles the AD phenotype in patients, including inflammatory parameters, barrier dysfunction, itch, and histopathological characteristics, providing a novel platform to evaluate targets for the treatment and prevention of AD. Furthermore, this model exposed the cells and cytokines that are critically associated with disease severity, including eosinophils, mast cells, TSLP, IL-4 and IL-9, but not CD4+ T cells. The instrumental role of these effector cells and cytokines was established by their stepwise depletion or blockade. Indeed, functional eosinophil depletion via the use of inducible eosinophil (iPHIL) mice significantly ameliorated AD pathology, most notably itch. Similar results were obtained after blockade of the IL-4/IL-13 axis by genetic deletion of STAT6. The clinically more relevant use of soluble inhibitors targeting IL-9 and CRTh2 (in a prophylactic and therapeutic setting, respectively), both resulted in a substantial reduction in AD phenotype. In summary, this body of work led to the identification of key disease-initiating and effector cells and molecules that represent attractive targets for the treatment of AD.</p>



2016 ◽  
Vol 13 (3) ◽  
pp. 59-64
Author(s):  
O G Elisyutina ◽  
O V Shtyrbul ◽  
E N Zemskaya

Atopic dermatitis is chronic inflammatory multifactorial disease, which has genetic disorders, immune mechanisms of development and is under the ainfluence of a combination of exogenous and endogenous factors. Recently a leading role of the epidermal barrier dysfunction in the pathogenesis of atopic dermatitis was shown. The article presents data about emollient for skin care efficacy - Cetaphil® RESTORADERM, which consists of preceramides and filaggrin breakdown products in complex treatment of atopic dermatitis patients.



2014 ◽  
Vol 11 (4) ◽  
pp. 59-63
Author(s):  
E T KINDEEVA ◽  
N G KOROTKII ◽  
A N PAMPURA

Background. Structural and functional damages of the epidermal barrier in patients with atopic dermatitis promote the entry of allergens and development of Th2-type allergic inflammation. Moisturizers containing lipids increase the physiological antiinflammatory effects of topical corticosteroids (TGKS), improve the epidermal barrier and reduce the duration of TGKS using preventing further infringement barrier. To evaluate the clinical efficacy of emollient milk Xemose in children with atopic dermatitis. Materials and methods. We examined 27 children with atopic dermatitis. Children were divided into 2 groups: patients in group 1 (n=14) used emollient milk Xemose twice a day on the skin lesions and limbs in the complex therapy, patients in the 2nd group (n=13) received combined therapy incorporating traditional dampening agents on the basis of lanolin (Unna cream) 3 times daily. All patients underwent measurement of transepidermal water loss (TEWl) (Tewameter TM 300, Multi Probe Adapter MPA 5/9, Courage + Khazaka) and the pH of the skin (Skin-pH-Meter, Multi Probe Adapter MPA 5/9, Courage + Khazaka) before and after 2 weeks of therapy. Results. Patients in groupthat used Xemose milk and children in group with Unna cream after 2 weeks showed a statistically significant decrease of TEWl (p=0,041 and p=0,04, respectively). TEWl was significantly lower in children treated for 2 weeks with milk Xemose (p=0,027) than in children treated with Unna cream. in both groups pH skin surface have not changed (р=0,22 and р=0,22 respectively). Conclusion. Clinical efficacy of milk Xemose as compound improving skin barrier function in children with atopic dermatitis was shown.



2020 ◽  
Vol 19 (6) ◽  
pp. 432-443
Author(s):  
Nikolay N. Murashkin ◽  
Leyla S. Namazova-Baranova ◽  
Leonid A. Opryatin ◽  
Roman V. Epishev ◽  
Alexander I. Materikin ◽  
...  

Atopic dermatitis (AD) is the disease with chronic inflammation, epidermal barrier dysfunction and microbial dysbiosis. AD is widespread, including pediatric population. The article discusses the disease’s pathogenesis: skin barrier deficiency, immunological causes of chronic inflammation, characteristics of normal skin microbiome and its disorders on both affected and unaffected skin of children with AD. Main principles of systemic treatment for moderate and severe forms of disease are considered. Features of targeted therapy with dupilumab (IL 4/IL 13 inhibitor) in children with moderate and severe forms of AD are discussed. The overview of the research results on the dupilumab efficacy and safety is presented.



2019 ◽  
Vol 11 (480) ◽  
pp. eaav2685 ◽  
Author(s):  
Donald Y. M. Leung ◽  
Agustin Calatroni ◽  
Livia S. Zaramela ◽  
Petra K. LeBeau ◽  
Nathan Dyjack ◽  
...  

Skin barrier dysfunction has been reported in both atopic dermatitis (AD) and food allergy (FA). However, only one-third of patients with AD have FA. The purpose of this study was to use a minimally invasive skin tape strip sampling method and a multiomics approach to determine whether children with AD and FA (AD FA+) have stratum corneum (SC) abnormalities that distinguish them from AD without FA (AD FA−) and nonatopic (NA) controls. Transepidermal water loss was found to be increased in AD FA+. Filaggrin and the proportion of ω-hydroxy fatty acid sphingosine ceramide content in nonlesional skin of children with AD FA+ were substantially lower than in AD FA− and NA skin. These abnormalities correlated with morphologic changes in epidermal lamellar bilayer architecture responsible for barrier homeostasis. Shotgun metagenomic studies revealed that the nonlesional skin of AD FA+ had increased abundance of Staphylococcus aureus compared to NA. Increased expression of keratins 5, 14, and 16 indicative of hyperproliferative keratinocytes was observed in the SC of AD FA+. The skin transcriptome of AD FA+ had increased gene expression for dendritic cells and type 2 immune pathways. A network analysis revealed keratins 5, 14, and 16 were positively correlated with AD FA+, whereas filaggrin breakdown products were negatively correlated with AD FA+. These data suggest that the most superficial compartment of nonlesional skin in AD FA+ has unique properties associated with an immature skin barrier and type 2 immune activation.



2021 ◽  
Vol 12 ◽  
pp. 204062232110583
Author(s):  
Silvia Ferrucci ◽  
Maurizio Romagnuolo ◽  
Carlo Alberto Maronese ◽  
Francesca Germiniasi ◽  
Simona Tavecchio ◽  
...  

Background: Atopic dermatitis (AD) is a common chronic-relapsing inflammatory skin disease hallmarked by epidermal barrier dysfunction, increased transepidermal water loss (TEWL) and decreased skin hydration. Recent findings on the T helper 2 (Th2)-driven pathogenesis of AD have led to the development of dupilumab, a monoclonal antibody directed against interleukin-4 and interleukin-13 that has been demonstrated to be effective in the treatment of moderate-to-severe AD. The effect of dupilumab on skin barrier dysfunction, however, has not yet been adequately investigated. Objectives: The primary endpoint of this study was to assess the status of the skin barrier in nonlesional skin of patients with severe AD treated with dupilumab, by evaluating the association between the relative variation of TEWL and the achievement of a 75% reduction of EASI (EASI75) over time. Methods: TEWL was measured below the antecubital fossae by means of the Vapometer® at baseline, at week 4 (T4), at week 16 (T16) and at week 32 after dupilumab starting. EASI and NRS-itch were measured at the same time points. Results: Seventy-eight patients with severe AD treated with dupilumab were enrolled. Median TEWL relative variation respect to baseline was significantly higher in patients who achieved EASI75 as compared with those who did not achieve EASI75 at T16 and at T32, but not at T4. Conclusion: During dupilumab treatment, TEWL on nonlesional skin tends to significantly improve 4 months after treatment initiation and could be a good tool for monitoring response to therapy.



2020 ◽  
Author(s):  
Aayushi Uberoi ◽  
Casey Bartow-McKenney ◽  
Qi Zheng ◽  
Laurice Flowers ◽  
Amy Campbell ◽  
...  

SUMMARYThe epidermis forms a barrier that defends the body from desiccation and entry of harmful substances, while sensing and integrating environmental signals. The tightly orchestrated cellular changes required for the proper formation and maintenance of this epidermal barrier occur in the context of the skin microbiome. Using germ free mice, we demonstrate the microbiota is necessary for proper differentiation and repair of the epidermal barrier. These effects were mediated by the aryl hydrocarbon receptor (AHR) in keratinocytes, a xenobiotic receptor also implicated in epidermal differentiation. Murine skin lacking keratinocyte AHR was more susceptible to barrier damage and infection, during steady state and epicutaneous sensitization. Colonization with a defined consortium of human skin isolates restored barrier competence in an AHR-dependent manner. We reveal a fundamental mechanism whereby the microbiota regulates skin barrier formation and repair, with far-reaching implications for the numerous skin disorders characterized by epidermal barrier dysfunction.



Sign in / Sign up

Export Citation Format

Share Document