HBD1 and LL37 gene expression in children with atopic dermatitis

E. Bystritskaya, N. Murashkin, A. I. Materikin, E. Naumova, I. V. Yakovleva, N. Vartanova, O. Svitich
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Abstract

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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HBD1和LL37基因在儿童特应性皮炎中的表达
特应性皮炎(AD)是一种多因素遗传决定的炎症性皮肤病,其特征是瘙痒、慢性病程、与年龄相关的定位特征和病变形态。特应性皮炎是由遗传、免疫和环境因素的复杂相互作用引起的。皮肤的屏障功能在特应性皮炎中受损。抗菌肽,如LL-37, b防御素参与维持皮肤屏障功能(特别是细胞间接触)。抗菌肽的失衡可能导致不同的疾病,包括过敏性疾病。本研究的目的是研究中、重度特应性皮炎患儿治疗前后皮肤和血液单个核细胞样本中编码抗菌肽的HBD1和LL37基因表达谱。通过实时聚合酶链反应检测HBD1和LL37基因的表达水平。统计学分析显示,两组患者HBD1表达水平均显著升高(p 0.017) (H-test = 24.76;2, n = 72;p = 0.00001), LL37基因(H-test = 15.69;2, n = 72;p = 0.00039),以及与对照组相比,受影响皮肤中HBD1表达水平降低(p 0.05)。我们关于皮肤中cathelicidin基因的数据与文献数据没有差异,因为它在AD中的表达减少。在我们的系列研究中,pbmc中基因表达增加。HBD1肽在单核细胞和巨噬细胞中均表达,代表先天免疫和适应性免疫之间的联系。在我们的研究中,HBD1基因的表达仅在血液中增加,这表明在炎症反应中,在全身水平上激活了先天免疫成分。重要的是,了解免疫标记物在AD中的作用将有助于开发新的治疗特应性疾病患者的预后方法。因此,应了解变态反应性疾病的发病机制。
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