Role of skin antimicrobial peptides in the pathogenesis of psoriasis, atopic dermatitis and hidradenitis suppurative: Highlights on dermcidin

José E Belizário
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Abstract

Diverse classes of antimicrobial peptides (AMPs) produced by keratinocytes, sebocytes, epithelial cells of apocrine and eccrine sweat glands and innate immune cells are continually released in the skin tissue layers. Together they exert the fine homeostatic control of the host immune cells-skin microbiome interactions, inhibiting bacterial overgrowth and skin barrier disruption. Under a variety of pathological conditions, up or down regulation of AMP expression can contribute to microbial diversity imbalance or dysbiosis, which can initiate or worsen the most common cutaneous diseases. This review updates on the roles of dermcidin, defensins, cathelicidins and S100 proteins as modulators of microbiomes, inflammation and recurrent bacterial infections in psoriasis, atopic dermatitis and hidradenitis suppurativa. The top most significant disease-immune signaling pathways mediated by the cytokines IL-1, TNF-α, IL-17, IL-23 and IL-33 are also reviewed. Current studies suggest that raising and lowering of host cell- and bacterial-derived AMPs may directly affect microbiome and immunity homeostasis at local body sites. Molecular genetics and microbiome studies should help us to investigate the bacterial species and AMPs synergistic or harmful interactions with causal gene variants, harnessing their potential clinical application in the journey of skin disease patients.
皮肤抗菌肽在银屑病、特应性皮炎和化脓性汗腺炎发病机制中的作用:皮肤抗菌肽研究综述
由角质形成细胞、皮脂细胞、大汗腺和汗腺上皮细胞以及先天免疫细胞产生的各种抗菌肽(AMPs)在皮肤组织层中不断释放。它们共同发挥宿主免疫细胞-皮肤微生物组相互作用的精细稳态控制,抑制细菌过度生长和皮肤屏障破坏。在多种病理条件下,AMP表达的上调或下调可导致微生物多样性失衡或生态失调,从而引发或加重最常见的皮肤疾病。本文综述了在银屑病、特应性皮炎和化脓性汗腺炎中,杀皮素、防御素、抗菌素和S100蛋白作为微生物组、炎症和复发性细菌感染调节剂的作用。综述了IL-1、TNF-α、IL-17、IL-23和IL-33等细胞因子介导的最重要的疾病免疫信号通路。目前的研究表明,宿主细胞和细菌来源的amp的升高和降低可能直接影响局部身体部位的微生物组和免疫稳态。分子遗传学和微生物组研究将有助于我们调查细菌种类和amp与致病基因变异的增效或有害相互作用,利用它们在皮肤病患者旅程中的潜在临床应用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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