The permeability barrier in the epidermis of the grass snake during the resting stage of the sloughing cycle

Landmann, Lukas; Stolinski, C.; Martin, Bruce D.

doi:10.1007/bf00239121

Cited by 53 publications

(24 citation statements)

References 32 publications

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“…In the non-keratinized epidermis of fish and amphibian tadpoles, TJs separate the body from the external aquatic environment (18,19). In terrestrial vertebrates, in which stratum corneum (SC) evolved presumably as an air-liquid interface barrier to avoid desiccation as animals adapted to living in contact with air, TJ barriers exist covertly under the SC barriers (18,(20)(21)(22)(23)(24). They compartmentalize the epidermal extracellular fluid environment into two parts in mammals (described below) and possibly also in reptiles and birds ( Figure 1B).…”

Section: The Three Musketeers Of the Epidermal Barriermentioning

confidence: 99%

Epidermal barrier dysfunction and cutaneous sensitization in atopic diseases

Kubo¹,

Nagao²,

Amagai³

2012

J. Clin. Invest.

318

296

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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: The Three Musketeers Of the Epidermal Barriermentioning

confidence: 99%

Epidermal barrier dysfunction and cutaneous sensitization in atopic diseases

Kubo¹,

Nagao²,

Amagai³

2012

J. Clin. Invest.

318

296

View full text Add to dashboard Cite

show abstract

“…Beneath the mucus or SC, apical intercellular spaces of the living stratified epidermal cells are sealed with tight junctions (TJs) that limit paracellular leakage of water and electrolytes to maintain fluid homeostasis Tsukita and Furuse, 2002). The existence of TJ barriers in epidermis has been reported in fish, amphibians, reptiles, and, recently, in mammals (Farquhar and Palade, 1965;Mittal and Whitear, 1979;Landmann et al, 1981;Brandner et al, 2002). The knockout study of claudin-1, a TJ-specific integral membrane protein, demonstrated that TJs function as paracellular diffusion barriers in mammalian epidermis .…”

Section: Br Ief Definitive Repor Tmentioning

confidence: 99%

External antigen uptake by Langerhans cells with reorganization of epidermal tight junction barriers

Kubo¹,

Nagao²,

Yokouchi³

et al. 2009

J Cell Biol

143

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“…The mesos layer consists of multiple layers of alternating keratin and lamellar lipids, forming a laminated structure sandwiched between the ␤-and ␣-keratin of the mature stratum corneum (Figs·1, 2, 3B) (Lillywhite and Maderson, 1982). The lipid sheets of the mesos layer prevent the outward flux of tracer molecules such as lanthanum and comprise the recognized water barrier in squamate reptiles (Landmann et al, 1981;Lillywhite and Maderson, 1982). The lipids concentrated in the reptilian mesos layer, as inferred from studies of shed epidermis, appear to be a complex mixture having a composition resembling that of the mammalian stratum corneum (consisting mostly of cholesterol, free fatty acids, phospholipids and ceramides: Lillywhite, 1980, 1983;Burken et al, 1985;Itoh et al, 1990;Elias and Menon, 1991;Weldon, 1996;Ball, 2004).…”

Section: Lipid Barriers Of Amphibiansmentioning

confidence: 99%