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PubMed2001

Characterisation of major and minor Dermatophagoides allergens in canine atopic dermatitis.

Atopic dermatitis is a well-recognised chronic inflammatory skin disease of humans and dogs. Most atopic dogs are sensitised to Dermatophagoides mites. The aim of this study was to characterise allergens in different Dermatophagoides species using polyclonal and monoclonal antibodies to canine IgE. Western blots were prepared from crude extracts of D farinae, D pteronyssinus and D microceras, and purified group 1 and 2 allergens under reducing and non-reducing conditions. They were probed with sera from atopic (n = 33) and healthy (n = 27) dogs. There was no significant difference in the sensitivity or specificity between the polyclonal and monoclonal sera in detecting Dermatophagoides -specific IgE. Major allergens common to both D farinae and D pteronyssinus were detected at 97-98 kDa, 103-104 kDa and 134-139 kDa on both reducing and non-reducing blots. Major allergens at 84-85 kDa, 65-69 kDa and 44-45 kDa were only recognised on reducing blots, suggesting that these are fragments of the larger allergens. Only a few sera recognised group 1 or 2 allergens on blots of crude extracts or purified allergens. These results confirm that, in atopic dogs, high molecular weight allergens are the most important Dermatophagoides allergens, rather than the low molecular weight group 1 and 2 proteins.

Animals↗

PubMed2007

[Specific immunotherapy in the treatment of atopic dermatitis].

Atopic dermatitis (AD) is a common chronic inflammatory skin disease that is part of the atopic syndrome and is frequently associated with asthma and allergic rhinoconjunctilitis. Acute eczematous lesions are characterized by erythema, cozing and crusting, whereas chronic lesions show thickened skin and papules. In addition to local and systemic therapy adjusted to the stage of the disease, the search for relevant trigger factors and consecutively their avoidance plays a crucial role in disease management. Aeroallergens like house-dust-mites, pollen and animal epithelia represent important trigger factors in sensitized patients. While allergen-specific immunotherapy (SIT) is widely and most effective used in allergy to insect venoms and allergic rhinitis, its use in AD is still controversial. Double-blind, placebo-controlled clinical trials show that SIT is effective in patients with AD and clinically relevant sensitization to house dust mites and grass pollen and leads to clinical improvement of eczema. Despite these encouraging data, the use of SIT as a routine therapeutic approach in AD requires further evaluation.

Dermatitis, Atopic↗

PubMed1997

[Atopic dermatitis].

Atopic dermatitis is a type of eczema determined by polygenic inheritance which is often associated with further phenotypes of the atopic syndrome such as extrinsic asthma and allergic rhinoconjunctivitis. Discussion of pathogenesis includes complex immunological and biochemical disorders as well as various triggering environmental factors. Characteristic patterns of distribution and morphology of the lesions vary with the patient's age. In addition, there is a broad spectrum of clinical variants. Diagnosis is based on stage-dependent eczematous morphology, if necessary validated by histology, family and personal history and clinical features of atopy, as well as on the results of allergologic assessment primarily comprising intra- and epicutaneous testing. Topical corticosteroids still are the main therapeutic approach.

Administration, Topical↗

PubMed2004

Malassezia yeasts in the pathogenesis of atopic dermatitis.

Atopic dermatitis is a common skin condition, the aetiology of which is multifactorial, involving genetic, immunological and environmental factors. In recent years, it has been suggested that various microbial organisms may also be involved in the pathogenesis of the disease. Yeasts belonging to the Malassezia genus have received particular attention. These yeasts, known to be a part of the normal skin flora, have been shown to be capable of inducing immunoglobulin (Ig)E-mediated and T-cell mediated immune responses postulated to contribute to chronic inflammation in the skin, particularly in the head and neck region, where colonization with Malassezia is the greatest. Considerable evidence now exists to support this idea, raising the possibility that specific antifungal therapy may be a useful treatment measure in some atopic patients who have a head and neck pattern of dermatitis.

Antifungal Agents↗

PubMed2000

The modulation of cytokine and IgE production by tumor necrosis factor-beta in atopic dermatitis.

Atopic dermatitis (AD) is associated with increased IL-4, IL-5, and IL-13 but decreased IFN-gamma production. This cytokine profile may account for the atopic features of this illness, including IgE upregulation. Recent studies have demonstrated that tumor necrosis factor (TNF)-beta is produced by Th1-like cells, but the cytokine modulation by TNF-beta and the clinical significance of this cytokine in AD is not known. Therefore, this study was carried out to determine the potential role of TNF-beta in AD. In this study, we cultured peripheral blood mononuclear cells from patients with AD and normal subjects with anti-CD3 monoclonal antibodies and investigated the production of TNF-beta by ELISA. The mean +/- SEM of TNF-beta production in AD was significantly lower than normal subjects (p = 0.03). The effect of TNF-beta on cytokine production was investigated by culturing peripheral blood mononuclear cells with anti-CD3 monoclonal antibodies in the presence or absence of TNF-beta. Compared with medium control, TNF-beta significantly decreased IL-5 (p = 0.0004) and IL-13 (p = 0.008) but increased IFN-gamma (p = 0.001) production. The effect of TNF-beta on IgE production was determined by culturing peripheral blood mononuclear cells in the IL-4- and anti-CD40-induced IgE production system. Interestingly, TNF-beta significantly decreased IgE (p = 0.02), but not IgG production compared with medium control. Our study demonstrates that TNF-beta production is downregulated in AD. This cytokine increases IFN-gamma production but decreases IL-5, IL-13, as well as IgE production. These findings suggest a potential role for TNF-beta in the pathogenesis of AD.

Adult↗

PubMed2000

Role of dysregulated apoptosis in atopic dermatitis.

Atopic dermatitis is a chronic inflammatory skin disease with a complex immune dysregulation and interplay of genetic, environmental and psychological factors. Activation and skin-selective homing of peripherial-blood T cells, and effector functions in the skin, represent sequential events in the pathogenesis. Dysregulated apoptosis in skin-homing T cells, eosinophils and keratinocytes contributes to the elicitation and persistence of atopic derrmatitis.

Animals↗

PubMed1990

[Pathogenesis and clinical aspects of atopic dermatitis].

Atopic dermatitis (a. D.) is a chronically relapsing inflammatory disease of the skin caused by a genetically transmitted hypersensitivity to environmental substances. Its pathogenesis is complex and multifactorial: heredity of atopic constitution, disturbances of humoral (hyperimmunoglobulinemia-E) and cellular (defect of suppressor-T-cells) immunity, abnormal vascular reactions and abnormal skin functions. A. D. shows different forms in different age groups: Eczema infantum in infancy, Eczema flexurarum in childhood and Neurodermatitis disseminata and pruriginosa while and after puberty. Typically for all forms is a pruritus and the status neurodermiticus. The healing of a. D. is spontaneously possible at any time, but not predictable for a special case.

Antibody Formation↗

PubMed1999

NC/Nga mice: a mouse model for atopic dermatitis.

Atopic dermatitis (AD) is a common pruritic disease that occurs primarily in infancy and childhood. AD is characterized by itching and the patient having an individual or family history of atopic diseases. Although AD is also frequently associated with elevated serum IgE levels and with common environmental factors contributing to its pathogenesis, the etiology of AD is still unknown. We examined NC/Nga mice (NC mice) that showed AD-like skin lesions with aging as a possible mouse model for AD. NC mice were maintained under conventional (Conv) or specific pathogen-free (SPF) conditions. Clinical symptoms, serum IgE levels and histopathology of the skin were compared between these 2 groups, and we explored their application as a model of human AD. It was found that the skin lesions of inbred NC mice were clinically and histologically very similar to human AD when the mice were raised under Conv conditions, but not under SPF conditions, and we assumed that some kinds of environmental factors might trigger AD-like signs and symptoms in NC mice. To further investigate the pathophysiology and treatment of AD, a suitable animal model is absolutely required, and NC mice are very useful for this purpose.

Aging↗

PubMed2004

The care of the child with atopic dermatitis.

Atopic dermatitis (AD) is one of the most common skin conditions in children. Its course is chronic and recurrent. The main symptom of AD is acute pruritus accompanying eczematous skin lesions. Care for the atopic child is an important element of complex therapy and the essential support for the pharmacological treatment. The aim of the care of the children with AD is to eliminate irritants and reduce such symptoms as dryness of skin, itch and sleep disturbances.

Adolescent↗

PubMed1986

Pharmacophysiology of atopic dermatitis.

Atopic dermatitis is clearly characterized by altered cutaneous physiologic responses. There is a tendency to acral vasoconstriction. Rubbing causes skin pallor and white dermographism. Vascular instability is demonstrated by responses to cholinergic agents, histamine, and nicotinates. Psychophysiologic studies demonstrate exaggerated vasodilator responses to emotional stress with consequent pruritus and scratching. The itch threshold is low, duration is prolonged, and nighttime scratching movements may be frequent or almost continuous. Regardless of the inciting trigger factors, the scratching causes the damage and the severe dermatitis. Thermal as well as emotional stimuli to sweating cause severe itching in AD, yet the concept of a miliaria-type, poral occlusion mechanism remains unproven. Some studies suggest actually increased sweating along with erythema and pruritus during acute flares of AD. The concept of sweat-borne allergens causing skin reactions during sweating is interesting but has never been proven. Studies of sweat responses to pharmacologic agents have produced conflicting data, and attempts to link these responses to Szentivanyi's beta-adrenergic blockade theory are not convincing. The numerous variables of climate, season, sex, age, and habitus affect sweating greatly. Future studies must carefully control for each of these factors before pharmacologically induced sweat responses can be interpreted clearly. A number of lines of evidence suggest involvement of histamine and other mediators in the evolution of erythema, pruritus, and scratching in AD. Flares of the condition have been reproducibly evoked by only two incitants: experimental emotional stress interviews and specific food challenge in selected sensitive individuals. In the latter, increased plasma histamine has been demonstrated, presumably generated by antigen/IgE stimulated degranulation of mast cells in the gut and/or skin. The demonstrated increased histamine releasability of basophils from atopic individuals may be the result of defective cellular regulatory mechanisms. Recent studies have demonstrated increased cyclic AMP-phosphodiesterase activity in leukocytes from atopic individuals. The resultant decreased intracellular cyclic AMP removes an inhibitory factor, which in turn causes net cellular hyperresponsiveness. This effect has been shown to account, at least in part, for increased histamine release from leukocytes of patients with AD. These and other studies focused upon cell functional regulation are providing better understanding of basic biochemical abnormalities and may lead to improved diagnostic and therapeutic approaches in managing atopic disease.

Biofeedback, Psychology↗

PubMed2006

Atopic dermatitis.

Atopic dermatitis (AD) is an eczematous, highly pruritic chronic inflammatory skin disease. It usually begins early in life and often occurs in people with a personal or family history of asthma and allergic rhinitis. The prevalence is high, especially in children,and it has been rising in recent decades, in parallel with asthma prevalence. Although AD is often described as an "allergic" dis-ease, allergic causation is difficult to document, and AD is increasingly viewed as a skin disease that predisposes to allergies. This interpretation, based on clinical, epidemiologic, and animal stu-dies, may greatly influence our approach to therapy and prevention of atopic diseases in the coming years.

Dermatitis, Atopic↗

PubMed1992

Dry skin in atopic dermatitis.

Atopic dermatitis (AD) is a common, chronically recurring skin disorder. Dry skin is a common finding in patients with AD, apart from the dermatitis. Although there are obvious clinical signs of an impaired barrier function of the skin, few investigators have studied this aspect of AD. The stratum corneum, where the barrier is located, has been studied with different techniques in patients with AD, and the results are now presented. The water-binding capacity of dry atopic skin was found to be reduced when measured with an in vitro microbalance technique. TEWL (transepidermal water loss) measured with and Evaporimeter Ep1, was increased in dry skin and in clinically normal skin of atopics on predilection areas. Water content was decreased in dry atopic skin, when measured with the Corneometer CM 420. In a quantitative electron microscopic study, the lamellar bodies were found to have an increased relative volume in dry atopic skin. When using chromatographic analysis, preliminary data suggested reduced amounts of extractable stratum corneum lipids in patients with AD. In a clinical study, 80% of the patients with AD regarded their skin as being dry. Fifty percent were found to have areas of dry skin, on clinical examination. By scanning electron microscopy (SEM), the surface pattern of dry atopic skin was found to be coarse and irregular. When using profilometry, quantitative differences in roughness parameters were found in dry atopic vis-à-vis to normal skin.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Water↗

PubMed1991

Abnormalities in epidermal lipid metabolism in patients with atopic dermatitis.

Atopic dermatitis is an inflammatory skin disease characterized by dryness and itch of the skin. In this study, we measured the phospholipid content and the fatty acid pattern of lesional and lesion-free epidermal keratome biopsies on 15 patients. For comparison, epidermal biopsies were obtained from healthy individuals undergoing plastic surgery. The phospholipid content of atopic epidermis was nearly twice as high as in healthy epidermis. Monounsaturated fatty acids in the phosphoglycerides were significantly increased (p less than 0.001) and n-6 fatty acids were significantly decreased (p less than 0.001) in lesional atopic epidermis compared to lesion-free epidermis. The content of esterified arachidonic acid in phosphatidylcholine from lesional epidermis was only 49% of that found in healthy epidermis (p less than 0.001). The content of free arachidonic acid was 47% higher (p less than 0.05), whereas the content of free long-chain saturated fatty acids was decreased by 29% (p less than 0.01), in lesional compared to lesion-free atopic epidermis. The disease severity, calculated as an arbitrary index, correlated inversely with the n-6 fatty acid content of lesion-free atopic epidermis (r = -0.89, p less than 0.001). Our findings suggest that atopic epidermis is characterized by an increased activity of phospholipase A2 and an incomplete transformation of phospholipids into other lipid classes.

Adult↗

PubMed1990

[Then physiopathology of atopic dermatitis].

Atopic dermatitis is transmitted as an autosomal dominant trait. Its expressivity is variable, and flare-ups are triggered by environmental factors such as air-borne allergens, cutaneous flora or foodstuffs. Elevation of serum IgE levels is inconstant and not specific; it is associated with a deficiency of suppressor T cell population. The epidermis contains IgE bound to the surface of Langerhans cells; this abnormality seems to be specific as it is not found in atopic or non atopic healthy subjects. The lack of beta-adrenergic response is partially explained by the hyperactivity of the cyclic AMP-degrading phosphodiesterase. Disturbances in essential fatty acid metabolism (inactivation of delta 6 desaturase) are thought to be responsible for abnormalities in the permeability of epithelial structures. The relationships between pharmacological, biochemical and immunological dysregulations are unknown.

Dermatitis, Atopic↗

PubMed2005

Lessons from murine models of atopic dermatitis.

Atopic dermatitis (AD) is a complex disease that manifests immunologic abnormalities in the skin. The immunologic changes of AD are characterized by a T helper cell type 2 (Th2)-dominated immune response in its acute phase and a Th1/Th2 mixed immune response in its chronic phase. Although the clinical presentation and pathologic changes are initially in the skin, AD may be, in part, a systemic disorder. In fact, AD is often considered to be the initial manifestation of the "atopic march" that progresses from AD to allergic rhinitis and asthma. In the past several years, a number of murine models of AD have been developed or discovered, and studies on these models have contributed greatly to our understanding of the immunopathogenesis of this disease. This review is focused on these recent, illuminating advances in animal models of AD.

Allergens↗

PubMed2002

Genetic association analysis using microsatellite markers in atopic dermatitis.

Atopic dermatitis (AD) is presumed to be influenced by genetic and environmental factors. In this study, 54 patients with AD were examined for disease association by the use of 12 microsatellite markers. Several significant associations were recognized in the alleles on chromosome 5, 7 and 11. AD genes were mapped near the FC epsilon RI beta gene (around D11S1314 locus) on chromosome 11, the IL4 gene cluster on chromosome 5 and the TCR gamma gene on chromosome 7. This distribution in close proximity to candidate loci for AD is very similar to that of atopic genes, therefore implying that an atopic trait is genetically responsible for the development of AD.

Adult↗

PubMedDate not supplied

The contribution of keratinocytes to the pathogenesis of atopic dermatitis.

Atopic dermatitis (AD) develops from a complex interplay between environmental, genetic, immunologic and biochemical factors. Relevant to the amplification and persistence of inflammatory and immune responses in AD skin are keratinocytes, which can be induced to secrete proinflammatory mediators in response to a variety of stimuli, including epidermal barrier perturbation. Moreover, keratinocytes from AD patients synthesize exaggerated amounts of mediators (e.g., GM-CSF and RANTES/CCL5) important for enhanced recruitment as well as sustained survival and activation of T cells and dendritic cells. AD keratinocytes have a constitutive dysregulated activity of transcription factors that modulate the expression of inflammatory genes, suggesting the existence of predetermined mechanisms targeting atopic inflammation to the skin. Among these, the existence of a defective epidermal barrier, which appears related to decreased ceramide generation and abnormal degradation of corneodesmosomes, certainly plays a central role in the predisposition to AD.

Cytokines↗

PubMedDate not supplied

Immune dysregulation in atopic dermatitis.

Atopic dermatitis (AD) is a chronic, relapsing, highly pruritic, inflammatory skin disease characterized by cutaneous hyperreactivity to environmentals triggers. Recent data suggest the presence of two different forms of AD: an extrinsic AD with elevated IgE involving 70-80% of the patients and an intrinsic AD with serum IgE not elevated and no specific IgE. Patients with extrinsic AD have elevated Th2- and decreased Thl-expressing cells in the peripheral blood, with elevated IL-4 and IL-13 expression, as well as IL-5. On the contrary, the intrinsic AD is linked with much lower levels of IL-4 and IL-13. Genetic factors are involved in the control of the disease and in the intrinsic AD the same chromosomal regions seem to be associated with psoriasis susceptibility. The AD is characterized by a complex of immunological alterations involving interactions between IgE-bearing antigen-presenting cells, T-cell activation, mast-cell degranulation, keratinocytes, eosinophils, and a combination of immediate and cellular immune responses. Inflammatory dendritic epidermal cells constitute a distinct dendritic cells population that is mainly found in AD and could induce the Th2/Thl isotopic switch contributing to AD chronic phase. Therapy is based on interventation in the pathophysiology of atopic eczema and elimination of exogenous provocation factors.

Animals↗