scholarly journals Comparing the Effect of a Twice-weekly Tacrolimus and Betamethasone Valerate Dose on the Subclinical Epidermal Barrier Defect in Atopic Dermatitis

2015 ◽  
Vol 95 (6) ◽  
pp. 653-658 ◽  
Author(s):  
J Chittock ◽  
K Brown ◽  
M Cork ◽  
S Danby
Cells ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 489 ◽  
Author(s):  
Géraldine Leman ◽  
Verena Moosbrugger-Martinz ◽  
Stefan Blunder ◽  
Petra Pavel ◽  
Sandrine Dubrac

Atopic dermatitis (AD) is characterized by dry and itchy skin evolving into disseminated skin lesions. AD is believed to result from a primary acquired or a genetically-induced epidermal barrier defect leading to immune hyper-responsiveness. Filaggrin (FLG) is a protein found in the cornified envelope of fully differentiated keratinocytes, referred to as corneocytes. Although FLG null mutations are strongly associated with AD, they are not sufficient to induce the disease. Moreover, most patients with ichthyosis vulgaris (IV), a monogenetic skin disease characterized by FLG homozygous, heterozygous, or compound heterozygous null mutations, display non-inflamed dry and scaly skin. Thus, all causes of epidermal barrier impairment in AD have not yet been identified, including those leading to the Th2-predominant inflammation observed in AD. Three dimensional organotypic cultures have emerged as valuable tools in skin research, replacing animal experimentation in many cases and precluding the need for repeated patient biopsies. Here, we review the results on IV and AD obtained with epidermal or skin equivalents and consider these findings in the context of human in vivo data. Further research utilizing complex models including immune cells and cutaneous innervation will enable finer dissection of the pathogenesis of AD and deepen our knowledge of epidermal biology.


2021 ◽  
Vol 22 (16) ◽  
pp. 8403
Author(s):  
Leszek Blicharz ◽  
Lidia Rudnicka ◽  
Joanna Czuwara ◽  
Anna Waśkiel-Burnat ◽  
Mohamad Goldust ◽  
...  

Atopic dermatitis (AD) is a common inflammatory dermatosis affecting up to 30% of children and 10% of adults worldwide. AD is primarily driven by an epidermal barrier defect which triggers immune dysregulation within the skin. According to recent research such phenomena are closely related to the microbial dysbiosis of the skin. There is growing evidence that cutaneous microbiota and bacterial biofilms negatively affect skin barrier function, contributing to the onset and exacerbation of AD. This review summarizes the latest data on the mechanisms leading to microbiome dysbiosis and biofilm formation in AD, and the influence of these phenomena on skin barrier function.


Author(s):  
Vasileva E.A. ◽  
Kuyarov A.A. ◽  
Kuyarov A.V.

The pathogenesis of atopic dermatitis (AD) is complex, and at present a unified concept of the development of the disease has not been formed. At the heart of pathogenesis, there is a complex interaction of numerous factors, such as genetic predisposition, dysfunction of the autonomic nervous system and the epidermal barrier. Previously, it has been proven that a high microbial contamination of the affected areas helps to maintain inflammation and aggravates skin dysfunction as a result of chronic inflammation, and favorable factors appear for the attachment of a secondary infection. However, little attention has been paid to dysfunctions of the epidermal barrier, the role of violations of the quantitative and qualitative composition of the microbiota in the development of AD, and this issue remains relevant at the present time. The aim of this study was to assess the effect of the carrier of bacteria on the mucous membranes of the upper respiratory tract in family members on the course of atopic dermatitis in a child. A bacteriological examination of the mucous membranes of the nose and throat was carried out in 34 children with AD and members of their families (74 people). When examining the mucous membranes of the nose and throat in family members of children with AD, it was found that the microflora isolated from family members in more than half of the cases has an increased potential for pathogenicity with a high degree of contamination (CFU lg 3), which forms an increased bacteriological load on the child. The tendency of bacterial carriage was revealed, contributing to the formation in the family of a permanent persistence of microflora with a high potential for pathogenicity. Asymptomatic carriage of bacteria forms an additional epidemiological load on the child, affects the severity of AD and is a risk factor in the development of secondary infection of the skin.


Author(s):  
Galina I. Smirnova

There are presented modern data describing the current understanding of the pathogenesis of atopic dermatitis (AD): a genetic predisposition to atopy, disruptions of epidermal barrier integrity and a cascade of immune responses, contributing allergic inflammation in the skin. There are both described several mechanisms of acute and chronic phases of AD, the main directions of pathogenetically substantiated treatment of AD in children and indicated the prospects of new preparations specific blockers of proinflammatory cytokines involved in the development of AD - crisaborole, apremilast, dupilumab, lebrikizumab, tralokinumab, tezepelumab. There is especially presented in details external therapy of atopic skin lesions in children with the use of means of modern dermatological cosmetics.


2014 ◽  
Vol 170 (4) ◽  
pp. 914-921 ◽  
Author(s):  
S.G. Danby ◽  
J. Chittock ◽  
K. Brown ◽  
L.H. Albenali ◽  
M.J. Cork

2019 ◽  
Vol 23 (3_suppl) ◽  
pp. 3S-13S ◽  
Author(s):  
Charles W. Lynde ◽  
James Bergman ◽  
Loretta Fiorillo ◽  
Lyn Guenther ◽  
Jill Keddy-Grant ◽  
...  

Atopic dermatitis (AD) is a chronic inflammatory skin condition, also referred to as atopic eczema, that is identified by itching and recurrent eczematous lesions. It often starts in infancy where it affects up to 20% of children but is also highly prevalent in adults. AD inflicts a significant psychosocial burden on patients and their families and increases the risk of other immune-mediated inflammatory conditions, such as asthma and allergic rhinitis, food allergy, and mental health disorders. It is a lifelong condition associated with epidermal barrier dysfunction and altered immune function. Through the use of emollients and anti-inflammatory agents, current prevention and treatment therapies attempt to restore epidermal barrier function. Acute flares are treated with topical corticosteroids. Topical calcineurin inhibitors (TCIs) and topical corticosteroids (TCSs) are used for proactive treatment to prevent remission. There remains a need and opportunity to improve AD care through future research directed toward an improved understanding of the heterogeneity of the disease and its subtypes, the role of autoimmunity in its pathogenesis, the mechanisms behind disease-associated itch and response to specific allergens, and the comparative effectiveness and safety of therapies.


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