Strain-Specific Phenotypes of Airway Inflammation and Bronchial Hyperresponsiveness Induced by Epicutaneous Allergen Sensitization in BALB/c and C57BL/6 Mice

Kodama, Motohiro; Asano, Koichiro; Oguma, Tsuyoshi; Kagawa, Shizuko; Tomomatsu, Katsuyoshi; Wakaki, Misa; Takihara, Takahisa; Ueda, Soichiro; Ohmori, Nao; Ogura, Hiromi; Miyata, Jun; Tanaka, Kyuto; Kamiishi, Nobufumi; Fukunaga, Koichi; Sayama, Koichi; Ikeda, Eiji; Miyasho, Taku; Ishizaka, Akitoshi

doi:10.1159/000312128

Cited by 24 publications

(20 citation statements)

References 34 publications

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“…Because filaggrin is not expressed in the upper airways (76), systemic sensitization is likely attributable to percutaneous antigen exposure through filaggrin-deficient skin. In good agreement with this hypothesis, percutaneous sensitization induces allergic responses to allergens in mice challenged via the upper airway (77,78). Further investigation is required to clarify the impact of filaggrin deficiency on the barrier function of SC and the molecular mechanisms of percutaneous sensitization in the pathophysiology of AD and atopic diseases.…”

Section: Major Players In Sc Barrier Dysfunctionmentioning

confidence: 65%

Epidermal barrier dysfunction and cutaneous sensitization in atopic diseases

Kubo¹,

Nagao²,

Amagai³

2012

J. Clin. Invest.

318

289

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Classic atopic dermatitis is complicated by asthma, allergic rhinitis, and food allergies, cumulatively referred to as atopic diseases. Recent discoveries of mutations in the filaggrin gene as predisposing factors for atopic diseases have refocused investigators' attention on epidermal barrier dysfunction as a causative mechanism. The skin's barrier function has three elements: the stratum corneum (air-liquid barrier), tight junctions (liquid-liquid barrier), and the Langerhans cell network (immunological barrier). Clarification of the molecular events underpinning epidermal barrier function and dysfunction should lead to a better understanding of the pathophysiological mechanisms of atopic diseases. IntroductionAtopic dermatitis (AD) is a chronic relapsing eczematous skin disorder that is frequently associated with elevated serum IgE levels and a family history of AD, allergic rhinitis, and/or asthma. Clinical manifestations of classic AD are dry skin and relapsing eczema, which usually start during early infancy or childhood and become complicated by food allergies, asthma, and/or allergic rhinitis during the first several years of life, in a process called "atopic march" (1). AD is highly prevalent in industrialized countries, where it affects approximately 15%-30% of children and 2%-10% of adults (2). The various observations of the disease indicate that AD has a complex etiology with genetic, immunological, and environmental aspects.Living organisms rely critically on surface barriers to isolate themselves from the external environment and to maintain homeostasis. While unicellular organisms are enclosed by cell membranes and cell walls, epithelial barrier structures, in several forms, cover the surfaces of multicellular organisms (3). In mammals, the airway and gastrointestinal tract are lined by simple epithelia covered with mucus. In contrast, the outer surface of the body is covered by a stratified epithelial cellular sheet called the epidermis, the outermost layer of which is cornified. Recent findings have shown that disruption of epithelial barrier systems are involved in the pathogenesis of immune disorders such as inflammatory bowel disease, asthma, and AD (4-12). In this review, we describe the barrier system of the epidermis, which is far more sophisticated than previously thought (13,14), and attempt to discuss its function with special focus on antigen penetration through these barriers and antigen capture by dendritic cells in the context of AD.

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Section: Major Players In Sc Barrier Dysfunctionmentioning

confidence: 65%

Epidermal barrier dysfunction and cutaneous sensitization in atopic diseases

Kubo¹,

Nagao²,

Amagai³

2012

J. Clin. Invest.

318

289

View full text Add to dashboard Cite

show abstract

“…As filaggrin is not expressed in the upper airways, systemic sensitization may be attributable to percutaneous antigen exposure via filaggrin‐deficient skin. In line with this hypothesis, percutaneous sensitization induces allergic responses to allergens in mice challenged via the upper airway …”

Section: Skin Barrier Dysfunctionmentioning

confidence: 66%

Atopic dermatitis: the skin barrier and beyond

et al. 2018

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Dysregulation of innate and adaptive immunity plays a key role; however, recent epidemiological, genetic and molecular research has focused interest on skin barrier dysfunction as a common precursor and pathological feature. Current understanding of the aetiology of atopic dermatitis highlights disruption of the epidermal barrier leading to increased permeability of the epidermis, pathological inflammation in the skin, and percutaneous sensitization to allergens. Thus, most novel treatment strategies seek to target specific aspects of the skin barrier or cutaneous inflammation. Several studies have also shown promise in preventing atopic dermatitis, such as the early use of emollients in high-risk infants. This may have broader implications in terms of halting the progression to atopic comorbidities including food allergy, hay fever and asthma.

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“…In this study, the BALB/c strain was chosen to develop a HWP allergy model because this strain has been recently used for transdermal sensitization models using peanuts , hazelnuts , and OVA as antigens. We are not aware of previous animal studies that examine the immune consequences of transdermal exposure to wheat proteins and HWP.…”

Section: Discussionmentioning

confidence: 99%