Department of Medical Microbiology, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey.
Institute of Graduate Studies in Health Sciences, Istanbul University, Istanbul, Turkey.
Arch Microbiol. 2024 Sep 20;206(10):410. doi: 10.1007/s00203-024-04134-w.
Atopic dermatitis (AD) is a common and recurrent skin disease characterized by skin barrier dysfunction, inflammation and chronic pruritus, with wide heterogeneity in terms of age of onset, clinical course and persistence over the lifespan. Although the pathogenesis of the disease are unclear, epidermal barrier dysfunction, immune and microbial dysregulation, and environmental factors are known to be critical etiologies in AD pathology. The skin microbiota represents an ecosystem consisting of numerous microbial species that interact with each other as well as host epithelial cells and immune cells. Although the skin microbiota benefits the host by supporting the basic functions of the skin and preventing the colonization of pathogens, disruption of the microbial balance (dysbiosis) can cause skin diseases such as AD. Although AD is a dermatological disease, recent evidence has shown that changes in microbiota composition in the skin and intestine contribute to the pathogenesis of AD. Environmental factors that contribute to skin barrier dysfunction and microbial dysbiosis in AD include allergens, diet, irritants, air pollution, epigenetics and microbial exposure. Knowing the microbial combination of intestin, as well as the genetic and epigenetic determinants associated with the development of autoantibodies, may help elucidate the pathophysiology of the disease. The skin of patients with AD is characterized by microbial dysbiosis as a result of reduced microbial diversity and overgrowth of the pathogens such as Staphylococcus aureus. Recent studies have revealed the importance of building a strong immune response against microorganisms during childhood and new mechanisms of microbial community dynamics in modulating the skin microbiome. Numerous microorganisms are reported to modulate host response through communication with keratinocytes, specific immune cells and adipocytes to improve skin health and barrier function. This growing insight into bioactive substances in the skin microbiota has led to novel biotherapeutic approaches targeting the skin surface for the treatment of AD. This review will provide an updated overview of the skin microbiota in AD and its complex interaction with immune response mechanisms, as well as explore possible underlying mechanisms in the pathogenesis of AD and provide insights into new therapeutic developments for the treatment of AD. It also focuses on restoring skin microbial homeostasis, aiming to reduce inflammation by repairing the skin barrier.
特应性皮炎（AD）是一种常见的复发性皮肤病，其特征为皮肤屏障功能障碍、炎症和慢性瘙痒，在发病年龄、临床过程和终生持续性方面具有广泛的异质性。尽管该疾病的发病机制尚不清楚，但已知表皮屏障功能障碍、免疫和微生物失调以及环境因素是 AD 病理生理学的关键病因。皮肤微生物组代表了一个由许多微生物物种组成的生态系统，这些物种相互作用，以及与宿主上皮细胞和免疫细胞相互作用。尽管皮肤微生物组通过支持皮肤的基本功能和防止病原体定植来使宿主受益，但微生物平衡的破坏（失调）可导致 AD 等皮肤病。虽然 AD 是一种皮肤病，但最近的证据表明，皮肤和肠道微生物群落组成的变化有助于 AD 的发病机制。导致 AD 皮肤屏障功能障碍和微生物失调的环境因素包括过敏原、饮食、刺激物、空气污染、表观遗传学和微生物暴露。了解肠道微生物组合以及与自身抗体发展相关的遗传和表观遗传决定因素，可能有助于阐明疾病的病理生理学。AD 患者的皮肤表现为微生物失调，表现为微生物多样性减少和金黄色葡萄球菌等病原体过度生长。最近的研究揭示了在儿童期建立针对微生物的强大免疫反应以及微生物群落动态调节皮肤微生物组的新机制的重要性。许多微生物通过与角质形成细胞、特定免疫细胞和脂肪细胞的通讯来调节宿主反应，从而改善皮肤健康和屏障功能，这一点已得到证实。对皮肤微生物组中生物活性物质的不断深入了解，导致了针对 AD 治疗的新型表面生物治疗方法。本综述将提供 AD 皮肤微生物组的最新概述及其与免疫反应机制的复杂相互作用，并探讨 AD 发病机制中的可能潜在机制，并为 AD 的治疗提供新的治疗发展思路。它还侧重于恢复皮肤微生物组稳态，旨在通过修复皮肤屏障来减少炎症。
