scholarly journals Current understanding of allergic march and the role of eczema in its development

2018 ◽  
Vol 72 ◽  
pp. 43-51
Author(s):  
Karolina Gwoździewicz ◽  
Ewa Cichocka-Jarosz
Keyword(s):  
Atopic Dermatitis ◽  
Subsequent Development ◽  
Childhood And Adolescence ◽  
Skin Microbiome ◽  
Atopic Diseases ◽  
Barrier Dysfunction ◽  
Atopic March ◽  
Leading Role ◽  
Typical Sequence

An increasing morbidity of atopic diseases (atopic dermatitis, food allergy, asthma and allergic rhinitis) documented in large cohort epidemiological studies is at least partially determined by high hygienic standards of living. Over the last 40 years, the accepted concept of pathogenesis of atopic diseases, the so-called atopic march, was proposed by Fouchard in 1973. It referred to the natural history of atopy manifestation, with a typical sequence of symptoms presented as atopic dermatitis in early childhood for subsequent development of allergic respiratory symptoms in late childhood and adolescence. New data suggests that the leading role of atopic dermatitis in atopic march might be less pronounced than previously expected, indicating coexistence rather than succession of atopic symptoms. The objective of this paper is to present the currently discussed concepts of atopic dermatitis – its pathogenesis, etiology, course and role in the development of other allergic diseases. More widely, we will present: 1. The genetic factors involved in skin barrier disruption with the leading role of loss-of-function gene for filaggrin mutation, 2. Genetic defects and epigenetic regulation of the immune system 3. Epidermal changes with physical barrier dysfunction as well as 4. Skin microbiome disturbances with Staphylococcus aureus colonization leading to abnormalities of the epidermal protective barrier.

scholarly journals The correction of epidermal barrier dysfunction in atopic dermatitis patients

2016 ◽  
Vol 13 (3) ◽  
pp. 59-64
Author(s):  
O G Elisyutina ◽  
O V Shtyrbul ◽  
E N Zemskaya
Keyword(s):  
Atopic Dermatitis ◽  
Genetic Disorders ◽  
Multifactorial Disease ◽  
Complex Treatment ◽  
Barrier Dysfunction ◽  
Epidermal Barrier ◽  
Endogenous Factors ◽  
Leading Role ◽  
Mechanisms Of Development

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.

scholarly journals Atopic dermatitis and vitamin D: facts and controversies

2013 ◽  
Vol 88 (6) ◽  
pp. 945-953 ◽  
Author(s):  
Kleyton de Carvalho Mesquita ◽  
Ana Carolina de Souza Machado Igreja ◽  
Izelda Maria Carvalho Costa
Keyword(s):  
Experimental Data ◽  
Vitamin D ◽  
Atopic Dermatitis ◽  
Immune Responses ◽  
Atopic Diseases ◽  
Barrier Dysfunction ◽  
Complex Interplay ◽  
The Past ◽  
Genetically Determined

Patients with atopic dermatitis have genetically determined risk factors that affect the barrier function of the skin and immune responses that interact with environmental factors. Clinically, this results in an intensely pruriginous and inflamed skin that allows the penetration of irritants and allergens and predisposes patients to colonization and infection by microorganisms. Among the various etiological factors responsible for the increased prevalence of atopic diseases over the past few decades, the role of vitamin D has been emphasized. As the pathogenesis of AD involves a complex interplay of epidermal barrier dysfunction and dysregulated immune response, and vitamin D is involved in both processes, it is reasonable to expect that vitamin D's status could be associated with atopic dermatitis' risk or severity. Such association is suggested by epidemiological and experimental data. In this review, we will discuss the evidence for and against this controversial relationship, emphasizing the possible etiopathogenic mechanisms involved.

scholarly journals THE ROLE OF GENETIC POLYMORPHISM OF THE FILAGGRIN PROTEIN WITH ATOPIC MARCH PROGRESSION IN CHILDREN

InterConf ◽  
2021 ◽  
pp. 187-200
Author(s):  
Tetiana Stoieva ◽  
Olesia Reshetilo ◽  
Natalia Vesilyk ◽  
Olha Portnova ◽  
Maksym Fedin ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Genetic Polymorphism ◽  
Gene Polymorphism ◽  
Life Quality ◽  
House Dust Mites ◽  
Control Group ◽  
Skin Microbiome ◽  
Atopic March ◽  
The Impact

The aim of the study. To determine the role of genetic polymorphism in the filaggrin gene R501XAA and 2282de4AA at atopic march progression in children. Materials and methods. 111 children aged 3 to 12 years with atopic dermatitis were selected and examined. As a result of genetic testing, it was found that 51 children with atopic dermatitis had polymorphism in the filaggrin gene. These patients were included in the main group. Another 60 children without polymorphism were in the control group. The filaggrin gene polymorphism was determined by examining the buccal epithelium by Dellaporta method. Sensitization to allergens was established on the basis of the specific IgE level. The impact of the disease on the quality of life of children was performed using the CDLQI questionnaire (Children's Dermatology Life Quality Index). Results. In the course of molecular genetics research, R501X mutation was detected in 40 ((78.4 ± 5.76)%) children, 2282del4 polymorphism – in 4 ((7.8 ± 3.76)%) patients, and their combined variant R501X + 2282del4 – in 7 (13%), (7 ± 4.81)% patients. When determining the effect of filaggrin polymorphism on the clinical course of atopic dermatitis, the presence of the associative relationship was established with the following indicators: the early onset of the disease – χ2 = 33.2, mostly severe course – χ2 = 16.2, severe skin dryness – χ2 = 22.6, predominant sensitization to fungi – χ2 = 10.6 and house dust mites – χ2 = 12.2, violation of the skin microbiome – χ2 = 7.8. Conclusions. Early manifestation of atopic dermatitis in children is associated with the filaggrin protein gene polymorphism ((82.4 ± 5.33)%), which determines the risk of progression of the atopic march and the development of bronchial asthma in (38.0 ± 6.8)% of children.

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
Keyword(s):  
At Risk ◽  
Atopic Dermatitis ◽  
Skin Barrier ◽  
Transepidermal Water Loss ◽  
Skin Microbiome ◽  
Children At Risk ◽  
Barrier Dysfunction ◽  
Epidermal Barrier ◽  
Microbiome Composition

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

scholarly journals The role of the skin microbiome in atopic dermatitis

2019 ◽  
Vol 122 (3) ◽  
pp. 263-269 ◽  
Author(s):  
Teruaki Nakatsuji ◽  
Richard L. Gallo
Keyword(s):  
Atopic Dermatitis ◽  
Skin Microbiome

scholarly journals Skin Barrier Abnormalities and Immune Dysfunction in Atopic Dermatitis

2020 ◽  
Vol 21 (8) ◽  
pp. 2867 ◽  
Author(s):  
Gabsik Yang ◽  
Jin Kyung Seok ◽  
Han Chang Kang ◽  
Yong-Yeon Cho ◽  
Hye Suk Lee ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Systemic Disease ◽  
Skin Barrier ◽  
Immune Dysregulation ◽  
Food Allergies ◽  
Atopic Diseases ◽  
Barrier Dysfunction ◽  
Underlying Mechanisms ◽  
Chronic Pruritus ◽  
And Function

Atopic dermatitis (AD) is a common and relapsing skin disease that is characterized by skin barrier dysfunction, inflammation, and chronic pruritus. While AD was previously thought to occur primarily in children, increasing evidence suggests that AD is more common in adults than previously assumed. Accumulating evidence from experimental, genetic, and clinical studies indicates that AD expression is a precondition for the later development of other atopic diseases, such as asthma, food allergies, and allergic rhinitis. Although the exact mechanisms of the disease pathogenesis remain unclear, it is evident that both cutaneous barrier dysfunction and immune dysregulation are critical etiologies of AD pathology. This review explores recent findings on AD and the possible underlying mechanisms involved in its pathogenesis, which is characterized by dysregulation of immunological and skin barrier integrity and function, supporting the idea that AD is a systemic disease. These findings provide further insights for therapeutic developments aiming to repair the skin barrier and decrease inflammation.

scholarly journals The role of the skin microbiome in atopic dermatitis: a systematic review

2017 ◽  
Vol 177 (5) ◽  
pp. 1272-1278 ◽  
Author(s):  
R.D. Bjerre ◽  
J. Bandier ◽  
L. Skov ◽  
L. Engstrand ◽  
J.D. Johansen
Keyword(s):  
Systematic Review ◽  
Atopic Dermatitis ◽  
Skin Microbiome

scholarly journals Epidermal Barrier Dysfunction in Atopic Dermatitis

2021 ◽  
Vol 79 (3) ◽  
pp. 207-216
Author(s):  
Tiago Fernandes Gomes ◽  
Rebeca Calado ◽  
Margarida Gonçalo
Keyword(s):  
Atopic Dermatitis ◽  
Current Knowledge ◽  
Skin Barrier ◽  
Initial Step ◽  
Barrier Dysfunction ◽  
Epidermal Barrier ◽  
Atopic March ◽  
T Helper 2 ◽  
Barrier Repair

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.  

scholarly journals Characterisation of the immune cells and cytokines involved in a model of atopic dermatitis

2021 ◽  
Author(s):  
◽  
Karmella Naidoo
Keyword(s):  
Atopic Dermatitis ◽  
Wide Spectrum ◽  
Management Strategies ◽  
Substantial Reduction ◽  
Skin Barrier ◽  
Barrier Dysfunction ◽  
Effector Cells ◽  
Treatment And Prevention ◽  
Inflammatory Parameters

<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>

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