揭示病毒诱导哮喘加重的机制:上皮损伤、免疫失调和新的干预措施

Xizi Du , Ming Yang
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引用次数: 0

摘要

病毒感染占哮喘加重(AE)的60 - 80% %,是儿科和成人人群的主要负担。病毒诱导的哮喘加重(VAE)的发病机制复杂,涉及上皮完整性破坏、干扰素反应缺陷和免疫细胞(如巨噬细胞和先天淋巴样细胞)的异常激活。此外,在病毒感染期间,2型(T2)和非T2炎症之间的相互作用受到动态调节,进一步放大气道功能障碍和重塑。虽然吸入皮质类固醇和靶向T2通路的生物制剂被广泛使用,但它们对VAE的疗效有限,特别是对嗜中性粒细胞或类固醇不敏感表型的患者,并且缺乏针对哮喘的病毒特异性抗病毒治疗。最近的进展强调了针对宿主免疫和上皮免疫相互作用的新方法,但大多数这些策略仍处于临床前或早期临床阶段,很少有个性化的治疗方法可用。本文综述了VAE发病机制和治疗进展,并讨论了靶向治疗策略发展的挑战和未来方向。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Unraveling the mechanisms of virus-induced asthma exacerbation: epithelial injury, immune dysregulation, and novel interventions
Viral infections account for 60–80 % of asthma exacerbations (AE), representing a major burden in both pediatric and adult populations. The pathogenesis of virus-induced asthma exacerbation (VAE) is mechanistically complex, involving disruption of epithelial integrity, defective interferon responses, and abnormal activation of immune cells such as macrophages and innate lymphoid cells. In addition, the interplay between type 2 (T2) and non-T2 inflammation is dynamically regulated during viral infections, further amplifying airway dysfunction and remodeling. Although inhaled corticosteroids and biologics targeting T2 pathways are widely used, their efficacy in VAE is limited, especially in patients with neutrophilic or steroid-insensitive phenotypes, and virus-specific antiviral therapies for asthma are lacking. Recent advances have highlighted novel approaches targeting host immunity and epithelial-immune interactions, but most of these strategies remain in preclinical or early clinical phases, with few personalized treatment approaches available. This review summarizes insights into VAE pathogenesis and therapeutic advances, and discusses challenges and future directions in the development of targeted therapeutic strategies.
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来源期刊
Chinese medical journal pulmonary and critical care medicine
Chinese medical journal pulmonary and critical care medicine Critical Care and Intensive Care Medicine, Infectious Diseases, Pulmonary and Respiratory Medicine
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0.40
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