The airway epithelium acts as a frontline defense against respiratory viruses, not only as a physical barrier and through the mucociliary apparatus but also through its immunological functions. It initiates multiple innate and adaptive immune mechanisms which are crucial for efficient antiviral responses. The interaction between respiratory viruses and airway epithelial cells results in production of antiviral substances, including type I and III interferons, lactoferrin, β-defensins, and nitric oxide, and also in production of cytokines and chemokines, which recruit inflammatory cells and influence adaptive immunity. These defense mechanisms usually result in rapid virus clearance. However, respiratory viruses elaborate strategies to evade antiviral mechanisms and immune responses. They may disrupt epithelial integrity through cytotoxic effects, increasing paracellular permeability and damaging epithelial repair mechanisms. In addition, they can interfere with immune responses by blocking interferon pathways and by subverting protective inflammatory responses toward detrimental ones. Finally, by inducing overt mucus secretion and mucostasis and by paving the way for bacterial infections, they favor lung damage and further impair host antiviral mechanisms.

中文翻译：

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气道上皮：与呼吸道病毒作斗争的士兵。

气道上皮作为抵御呼吸道病毒的前线防御，不仅作为物理屏障和通过黏液纤毛装置，而且通过其免疫功能。它启动多种先天性和适应性免疫机制，这对于有效的抗病毒反应至关重要。呼吸道病毒和气道上皮细胞之间的相互作用导致抗病毒物质的产生，包括 I 型和 III 型干扰素、乳铁蛋白、β-防御素和一氧化氮，以及细胞因子和趋化因子的产生，这些细胞因子和趋化因子会招募炎症细胞并影响适应性免疫. 这些防御机制通常会导致病毒快速清除。然而，呼吸道病毒制定了逃避抗病毒机制和免疫反应的策略。它们可能通过细胞毒性作用破坏上皮完整性，增加细胞旁通透性和破坏上皮修复机制。此外，它们可以通过阻断干扰素途径和破坏对有害途径的保护性炎症反应来干扰免疫反应。最后，通过诱导明显的粘液分泌和黏膜淤滞并为细菌感染铺平道路，它们有利于肺损伤并进一步削弱宿主的抗病毒机制。