HBD1 and LL37 gene expression in children with atopic dermatitis

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Atopic dermatitis (AD) is a multifactorial genetically determined inflammatory skin disease characterized by itching, chronic course, age-related features of localization and lesion morphology. Atopic dermatitis is caused by complex interactions between genetic, immunological, and environmental factors. The barrier function of the skin is impaired in atopic dermatitis. Antimicrobial peptides, e.g., LL-37, b-defensins are involved in maintaining the skin barrier function (especially, intercellular contacts). An imbalance of antimicrobial peptides may cause different disorders, including allergic pathologies. The aim of this study is to investigate gene expression profile of the HBD1 and LL37 encoding antimicrobial peptides in the samples of skin and blood mononuclear cells obtained from the children with moderate and severe atopic dermatitis before and after treatment. By means of real-time polymerase chain reaction, the levels of HBD1 and LL37 gene expression were evaluated in the samples. Statistical analysis showed significantly increased (p ≤ 0.017) expression levels of both HBD1 (H-test = 24.76; 2, n = 72; p = 0.00001), and LL37 genes (H-test = 15.69; 2, n = 72; p = 0.00039) in blood cells of AD patients compared to the control group, as well as decreased (p ≤ 0.05) levels of HBD1 expression in the affected skin compared to the control group. Our data on the cathelicidin gene in the skin do not differ from the literature data, since its expression is reduced in AD. In our series, an increase of the gene expression was revealed in PBMCs. The HBD1 peptide is expressed in both monocytes and macrophages, representing a link between innate and adaptive immunity. In our study, the expression of the HBD1 gene was increased only in blood, thus suggesting activation of innate immunity components at the systemic level in response to inflammation. Of importance, understanding the role of immunological markers in AD will help to develop novel prognostic approaches in management of the patients with atopic disorders. Therefore, one should understand pathogenetic mechanisms of allergic diseases.

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E. Bystritskaya

I. Mechnikov Research Institute for Vaccines and Sera

编辑信件的主要联系方式.
Email: lisabystritskaya@gmail.com

Postgraduate Student, Junior Research Associate, Laboratory of Molecular Immunology

俄罗斯联邦, Moscow

N. Murashkin

Medical Research Center for Children’s Health; I. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Sechenov University)

Email: lisabystritskaya@gmail.com

PhD, MD (Medicine), Professor, Senior Research Associate, Head, Department of Dermatology, Head, Laboratory of Skin Pathology in Children; Professor

俄罗斯联邦, Moscow; Moscow

Alexander Materikin

Medical Research Center for Children’s Health

Email: lisabystritskaya@gmail.com

PhD (Medicine), Dermatovenereologist, Department of Dermatology

俄罗斯联邦, Moscow

E. Naumova

M. Lomonosov Moscow State University

Email: lisabystritskaya@gmail.com

Research Associate, Department of Genetics, Faculty of Biology

俄罗斯联邦, Moscow

I. Yakovleva

I. Mechnikov Research Institute for Vaccines and Sera

Email: lisabystritskaya@gmail.com

PhD (Biology), Research Associate, Laboratory of Cells Hybridomas

俄罗斯联邦, Moscow

N. Vartanova

I. Mechnikov Research Institute for Vaccines and Sera

Email: lisabystritskaya@gmail.com

PhD (Biology), Senior Research Associate, Laboratory of Microbiology of Opportunistic Bacteria

俄罗斯联邦, Moscow

Oxana Svitich

I. Mechnikov Research Institute for Vaccines and Sera; I. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Sechenov University)

Email: lisabystritskaya@gmail.com

PhD, MD (Medicine), Corresponding Member, Russian Academy of Sciences, Head, Laboratory of Molecular Immunology, Director; Professor, Department of Microbiology, Virology and Immunology

俄罗斯联邦, Moscow; Moscow

参考

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版权所有 © Bystritskaya E.P., Murashkin N.N., Materikin A.I., Naumova E.A., Yakovleva I.V., Vartanova N.O., Svitich O.A., 2022

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