Department of Biological and Environmental Sciences, College of Arts and Sciences, Qatar University, Doha P.O. Box 2713, Qatar.
Laboratory of Animal Research Center (LARC), Qatar University, Doha P.O. Box 2713, Qatar.
Int J Mol Sci. 2023 Jul 24;24(14):11851. doi: 10.3390/ijms241411851.
Atopic dermatitis (AD) is the most common chronic relapsing neuroinflammatory skin disease that is characterized by a complex and multifactorial pathophysiology. It reflects a profound interplay between genetic and environmental factors, and a recently disclosed neuroimmune dysregulation that drives skin barrier disruption, pruritus, and microbial imbalance. In terms of the key external environmental players that impact AD, air quality and itch severity linkage have been thoroughly researched. The impact of ambient air pollutants including particulate matter (PM) and AD pruritic exacerbation has been recorded despite reductions in air pollution levels in in developed countries. The developing countries have, on the contrary, experienced significant urbanization and industrialization with limited environmental protection standards in the past decades. This unprecedented construction, petrochemical industry utilization, and increment in population counts has been paired with consistent exposure to outdoor PM. This may present a key cause of AD pruritic exacerbation supported by the fact that AD prevalence has intensified globally in the past 50 years, indicating that environmental exposure may act as a trigger that could flare up itch in vulnerable persons. At the molecular level, the impact of PM on severe pruritus in AD could be interpreted by the toxic effects on the complex neuroimmune pathways that govern this disease. AD has been recently viewed as a manifestation of the disruption of both the immune and neurological systems. In light of these facts, this current review aims to introduce the basic concepts of itch sensory circuits in the neuroimmune system. In addition, it describes the impact of PM on the potential neuroimmune pathways in AD pathogenesis with a special focus on the Fc Epsilon RI pathway. Finally, the review proposes potential treatment lines that could be targeted to alleviate pruritus based on immune mediators involved in the Fc Epsilon signaling map.
特应性皮炎（AD）是最常见的慢性复发性神经炎症性皮肤病，其特征是复杂的多因素病理生理学。它反映了遗传和环境因素之间的深刻相互作用，以及最近发现的神经免疫失调，导致皮肤屏障破坏、瘙痒和微生物失衡。就影响 AD 的关键外部环境因素而言，空气质量和瘙痒严重程度之间的联系已经得到了深入研究。尽管发达国家的空气污染水平有所降低，但环境空气中的污染物，包括颗粒物（PM）和 AD 瘙痒加重的影响已经被记录下来。相反，发展中国家在过去几十年经历了显著的城市化和工业化，而环境保护标准有限。这种前所未有的建设、石化工业利用和人口数量的增加，伴随着对户外 PM 的持续暴露。这可能是 AD 瘙痒加重的一个关键原因，因为过去 50 年来，AD 的全球患病率加剧，表明环境暴露可能作为一个触发因素，使易患人群的瘙痒加剧。从分子水平上讲，PM 对 AD 严重瘙痒的影响可以通过其对控制这种疾病的复杂神经免疫途径的毒性作用来解释。AD 最近被视为免疫系统和神经系统紊乱的表现。鉴于这些事实，本综述旨在介绍神经免疫系统中瘙痒感觉回路的基本概念。此外，它描述了 PM 对 AD 发病机制中潜在神经免疫途径的影响，特别关注 FcεRI 途径。最后，该综述提出了基于 Fcε信号通路图中涉及的免疫介质的潜在治疗方案，以减轻瘙痒。
