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      Relations between vitamin D3, total and specific IgE for house dust mites in atopic dermatitis patients

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          Abstract

          Atopic dermatitis (AD) is a chronic recurrent inflammatory skin disease. There are a lot of evidences on the importance of vitamin D and house dust mite (HDM) allergens in the etiology and course of AD. The objectives of this study are to evaluate the relation between vitamin D3 level and house dust mites (HDM) Dermatophagoidspecies sensitization in pathogenesis of atopic dermatitis. Cross-sectional design study was conducted on 50 atopic dermatitis patients. Blood analysis were done to determine level of vitamin D3, total IgE by fluorescent immunoassay & specific IgE for HDM (d1, d2) & other inhalant allergens by ELISA test. There was significant high negative correlation with the specific IgE for HDM (r =  −0. 62, p < 0.001) and vitamin D3. & there was non-significant minimal negative correlation with the specific IgE and other inhalant allergens (r = − 0.10, p > 0.05). There was a statistically significant relation between level of vitamin D3 and atopic dermatitis severity and sensitization to HDM and other allergens.

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          G*Power 3: A flexible statistical power analysis program for the social, behavioral, and biomedical sciences

          Franz Faul, Edgar Erdfelder, Albert-Georg Lang … (2007)
          G*Power (Erdfelder, Faul, & Buchner, 1996) was designed as a general stand-alone power analysis program for statistical tests commonly used in social and behavioral research. G*Power 3 is a major extension of, and improvement over, the previous versions. It runs on widely used computer platforms (i.e., Windows XP, Windows Vista, and Mac OS X 10.4) and covers many different statistical tests of the t, F, and chi2 test families. In addition, it includes power analyses for z tests and some exact tests. G*Power 3 provides improved effect size calculators and graphic options, supports both distribution-based and design-based input modes, and offers all types of power analyses in which users might be interested. Like its predecessors, G*Power 3 is free.
          Article 0 comments Cited 10303 times – based on 0 reviews     Review now
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            Injury enhances TLR2 function and antimicrobial peptide expression through a vitamin D-dependent mechanism.

            Jürgen Schauber, Robert A Dorschner, Alvin B Coda … (2007)
            An essential element of the innate immune response to injury is the capacity to recognize microbial invasion and stimulate production of antimicrobial peptides. We investigated how this process is controlled in the epidermis. Keratinocytes surrounding a wound increased expression of the genes coding for the microbial pattern recognition receptors CD14 and TLR2, complementing an increase in cathelicidin antimicrobial peptide expression. These genes were induced by 1,25(OH)2 vitamin D3 (1,25D3; its active form), suggesting a role for vitamin D3 in this process. How 1,25D3 could participate in the injury response was explained by findings that the levels of CYP27B1, which converts 25OH vitamin D3 (25D3) to active 1,25D3, were increased in wounds and induced in keratinocytes in response to TGF-beta1. Blocking the vitamin D receptor, inhibiting CYP27B1, or limiting 25D3 availability prevented TGF-beta1 from inducing cathelicidin, CD14, or TLR2 in human keratinocytes, while CYP27B1-deficient mice failed to increase CD14 expression following wounding. The functional consequence of these observations was confirmed by demonstrating that 1,25D3 enabled keratinocytes to recognize microbial components through TLR2 and respond by cathelicidin production. Thus, we demonstrate what we believe to be a previously unexpected role for vitamin D3 in innate immunity, enabling keratinocytes to recognize and respond to microbes and to protect wounds against infection.
            Article 0 comments Cited 156 times – based on 0 reviews     Review now
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              Basis for the barrier abnormality in atopic dermatitis: outside-inside-outside pathogenic mechanisms.

              Adrian Williams, Yutaka Hatano, Waldir P. Elias (2008)
              Until quite recently, the pathogenesis of atopic dermatitis (AD) has been attributed to primary abnormalities of the immune system. Intensive study revealed the key roles played by T(H)1/T(H)2 cell dysregulation, IgE production, mast cell hyperactivity, and dendritic cell signaling in the evolution of the chronic, pruritic, inflammatory dermatosis that characterizes AD. Accordingly, current therapy has been largely directed toward ameliorating T(H)2-mediated inflammation and pruritus. In this review we will assess emerging evidence that inflammation in AD results from inherited and acquired insults to the barrier and the therapeutic implications of this paradigm.
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                Author and article information

                Contributors
                Hassan M. Ibrahim: alhagazy1971@yahoo.com
                Journal
                Journal ID (nlm-ta): Sci Rep
                Journal ID (iso-abbrev): Sci Rep
                Title: Scientific Reports
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2045-2322
                Publication date (Electronic): 2 December 2020
                Publication date PMC-release: 2 December 2020
                Publication date Collection: 2020
                Volume: 10
                Electronic Location Identifier: 21000
                Affiliations
                [1 ]GRID grid.412707.7, ISNI 0000 0004 0621 7833, Dermatology, Andrology and Venereology, Qena Faculty of Medicine, , South Valley University, ; Qena, 83523 Egypt
                [2 ]GRID grid.417764.7, ISNI 0000 0004 4699 3028, Department of Dermatology, Andrology and Venereology, Aswan Faculty of Medicine, , Aswan University, ; Tingar, Egypt
                [3 ]GRID grid.412707.7, ISNI 0000 0004 0621 7833, Department of Medical Biochemistry, Qena Faculty of Medicine, , South Valley University, ; Qena, Egypt
                [4 ]GRID grid.412707.7, ISNI 0000 0004 0621 7833, Clinical Pathology, Qena Faculty of Medicine, , South Valley University, ; Qena, Egypt
                [5 ]GRID grid.412707.7, ISNI 0000 0004 0621 7833, Dermatology, Venereology and Andrology, Qena University Hospital, , South Valley University, ; Qena, Egypt
                [6 ]GRID grid.412707.7, ISNI 0000 0004 0621 7833, Parasitology Department, Qena Faculty of Medicine, , South Valley University, ; Qena, Egypt
                [7 ]GRID grid.412707.7, ISNI 0000 0004 0621 7833, Department of Dermatology, Andrology and Venereology, Qena Faculty of Medicine, , South Valley University, ; Qena, Egypt
                Article
                Publisher ID: 77968
                DOI: 10.1038/s41598-020-77968-1
                PMC ID: 7710713
                PubMed ID: 33268802
                SO-VID: c38a2b5d-bc53-4d43-bf80-37c479eaff6b
                Copyright © © The Author(s) 2020
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 9 July 2020
                Date accepted : 28 October 2020
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2020

                ScienceOpen disciplines: Uncategorized
                Keywords: biochemistry,immunology,medical research
                Data availability:
                ScienceOpen disciplines: Uncategorized
                Keywords: biochemistry, immunology, medical research

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