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      Atopic dermatitis in cats and dogs: a difficult disease for animals and owners

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          Abstract

          The purpose of this review article is to give an overview of atopic dermatitis in companion animals and of recent developments including knowledge on immunological background, novel treatment options and difficulties in disease management. The prevalence of hypersensitivities seems to be increasing. The pathogenetic mechanisms are not fully understood, yet multiple gene abnormalities and altered immunological processes are involved. In dogs and cats, the diagnosis of atopic dermatitis is based on history, clinical examination and exclusion of other differential diagnoses. Intradermal testing or testing for serum allergen-specific Immunoglobulin E is only used to identify allergens for inclusion in the extract for allergen immunotherapy. Symptomatic therapy includes glucocorticoids, ciclosporin, essential fatty acids and antihistamines. A selective janus kinase 1 inhibitor and a caninized monoclonal interleukin-31 antibody are the newest options for symptomatic treatment, although longterm effects still need to be assessed. The chronic and often severe nature of the disease, the costly diagnostic workup, frequent clinical flares and lifelong treatment are challenging for owners, pets and veterinarians. Patience and excellent communication skills are needed to achieve a good owner compliance and satisfactory clinical outcome for the animal.

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          Most cited references162

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          IL-25 induces IL-4, IL-5, and IL-13 and Th2-associated pathologies in vivo.

          We have characterized a cytokine produced by Th2 cells, designated as IL-25. Infusion of mice with IL-25 induced IL-4, IL-5, and IL-13 gene expression. The induction of these cytokines resulted in Th2-like responses marked by increased serum IgE, IgG(1), and IgA levels, blood eosinophilia, and pathological changes in the lungs and digestive tract that included eosinophilic infiltrates, increased mucus production, and epithelial cell hyperplasia/hypertrophy. In addition, our studies show that IL-25 induces Th2-type cytokine production by accessory cells that are MHC class II(high), CD11c(dull), and lineage(-). These results suggest that IL-25, derived from Th2 T cells, is capable of amplifying allergic type inflammatory responses by its actions on other cell types.
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            IL-25 augments type 2 immune responses by enhancing the expansion and functions of TSLP-DC–activated Th2 memory cells

            Interleukin (IL) 25 (IL-17E), a distinct member of the IL-17 cytokine family, plays important roles in evoking T helper type 2 (Th2) cell–mediated inflammation that features the infiltrations of eosinophils and Th2 memory cells. However, the cellular sources, target cells, and underlying mechanisms remain elusive in humans. We demonstrate that human Th2 memory cells expressing distinctive levels of IL-25 receptor (R) are one of the responding cell types. IL-25 promotes cell expansion and Th2 cytokine production when Th2 central memory cells are stimulated with thymic stromal lymphopoietin (TSLP)–activated dendritic cells (DCs), homeostatic cytokines, or T cell receptor for antigen triggering. The enhanced functions of Th2 memory cells induced by IL-25 are associated with sustained expression of GATA-3, c-MAF, and JunB in an IL-4–independent manner. Although keratinocytes, mast cells, eosinophils, and basophils express IL-25 transcripts, activated eosinophils and basophils from normal and atopic subjects were found to secrete bioactive IL-25 protein, which augments the functions of Th2 memory cells. Elevated expression of IL-25 and IL-25R transcripts was observed in asthmatic lung tissues and atopic dermatitis skin lesions, linking their possible roles with exacerbated allergic disorders. Our results provide a plausible explanation that IL-25 produced by innate effector eosinophils and basophils may augment the allergic inflammation by enhancing the maintenance and functions of adaptive Th2 memory cells.
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              The allergy epidemics: 1870-2010.

              Before the first description of hay fever in 1870, there was very little awareness of allergic disease, which is actually similar to the situation in prehygiene villages in Africa today. The best explanation for the appearance and subsequent increase in hay fever at that time is the combination of hygiene and increased pollen secondary to changes in agriculture. However, it is important to remember that the major changes in hygiene in Northern Europe and the United States were complete by 1920. Asthma in children did not start to increase until 1960, but by 1990, it had clearly increased to epidemic numbers in all countries where children had adopted an indoor lifestyle. There are many features of the move indoors that could have played a role; these include increased sensitization to indoor allergens, diet, and decreased physical activity, as well as the effects of prolonged periods of shallow breathing. Since 1990, there has been a remarkable increase in food allergy, which has now reached epidemic numbers. Peanut has played a major role in the food epidemic, and there is increasing evidence that sensitization to peanut can occur through the skin. This suggests the possibility that changes in lifestyle in the last 20 years could have influenced the permeability of the skin. Overall, the important conclusion is that sequential changes in lifestyle have led to increases in different forms of allergic disease. Equally, it is clear that the consequences of hygiene, indoor entertainment, and changes in diet or physical activity have never been predicted.
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                Author and article information

                Contributors
                ngedon@hotmail.de
                R.Mueller@lmu.de
                Journal
                Clin Transl Allergy
                Clin Transl Allergy
                Clinical and Translational Allergy
                BioMed Central (London )
                2045-7022
                5 October 2018
                5 October 2018
                2018
                : 8
                : 41
                Affiliations
                ISNI 0000 0004 1936 973X, GRID grid.5252.0, Small Animal Medicine Clinic, Centre for Clinical Veterinary Medicine, , Ludwig Maximilian University, ; Veterinaerstraße 13, 80539 Munich, Germany
                Article
                228
                10.1186/s13601-018-0228-5
                6172809
                30323921
                2c28595e-a509-410d-b325-bf2ab73f7071
                © The Author(s) 2018

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 2 July 2018
                : 10 September 2018
                Categories
                Review
                Custom metadata
                © The Author(s) 2018

                Immunology
                allergy,canine,feline,atopy-like dermatitis,adverse food reaction,il-31,lokivetmab,immunotherapy
                Immunology
                allergy, canine, feline, atopy-like dermatitis, adverse food reaction, il-31, lokivetmab, immunotherapy

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