Darlenski Razvigor, Kozyrskyj Anita L, Fluhr Joachim W, Caraballo Luis
Department of Dermatovenerology, ACC Tokuda Hospital, Sofia, Bulgaria; Department of Dermatovenerology, Trakia University, Stara Zagora, Bulgaria.
Department of Pediatrics, Faculty of Medicine and Dentistry, Edmonton Clinic Health Academy, Edmonton, Alberta, Canada.
J Allergy Clin Immunol. 2021 Dec;148(6):1387-1393. doi: 10.1016/j.jaci.2021.10.002. Epub 2021 Oct 28.
Atopic diathesis encompassing atopic dermatitis (AD), allergic rhinoconjunctivitis, food allergy, eosinophilic esophagitis, and asthma is a widely prevalent condition with a broad heterogeneity in clinical course, age of onset, and lifespan persistence. A primary event in AD is the commonly inherited epidermal barrier dysfunction. Together with the host-microbiome interactions, barrier defect and allergen exposure modulate both innate and adaptive immunity, thus triggering and maintaining the inflammatory response. Microbiome diversity, together with the host's contact with nonpathogenic microbes in childhood, is a prerequisite for functional maturation of the immune system, which is in part mediated by microbiome-induced epigenetic changes. Yet, whether microbiome alterations are the result or the reason for barrier impairment and inflammatory response of the host is unclear. Exposure to locally prevalent microbial species could contribute to further modification of the disease course. The objective of this review is to reveal the link between changes in the skin microbiota, barrier dysfunction, and inflammation in AD. Addressing unmet needs includes determining the genetic background of AD susceptibility; the epigenetic modifications induced by the microbiota and other environmental factors; the role of globally diverse provoking factors; and the implementation of personalized, phenotype-specific therapies such as a epidermal barrier restoration in infancy and microbiota modulation via systemic or topical interventions, all of which open gaps for future research.
特应性素质包括特应性皮炎（AD）、变应性鼻结膜炎、食物过敏、嗜酸性食管炎和哮喘，是一种广泛流行的疾病，在临床病程、发病年龄和病程持续时间方面具有广泛的异质性。AD的一个主要事件是常见的遗传性表皮屏障功能障碍。屏障缺陷和变应原暴露与宿主-微生物群相互作用一起，调节先天性和适应性免疫，从而触发并维持炎症反应。微生物群多样性以及宿主在儿童期与非致病性微生物的接触，是免疫系统功能成熟的先决条件，这部分是由微生物群诱导的表观遗传变化介导的。然而，尚不清楚微生物群改变是宿主屏障受损和炎症反应的结果还是原因。接触当地流行的微生物物种可能有助于疾病进程的进一步改变。本综述的目的是揭示皮肤微生物群变化、屏障功能障碍与AD炎症之间的联系。满足未满足的需求包括确定AD易感性的遗传背景；微生物群和其他环境因素诱导的表观遗传修饰；全球多样的激发因素的作用；以及实施个性化的、针对特定表型的治疗方法，如婴儿期的表皮屏障修复和通过全身或局部干预进行微生物群调节，所有这些都为未来的研究留下了空白。
