The mammalian lung has an enormous environmental-epithelial interface that is optimized to accomplish the principal function of the respiratory system, gas exchange. One consequence of evolving such a large surface area is that the lung epithelium is continuously exposed to toxins, irritants, and pathogens. Maintaining homeostasis in this environment requires a delicate balance of cellular signaling between the epithelium and innate immune system. Following injury, the epithelium can be either fully regenerated in form and function or repaired by forming dysplastic scar tissue. In this review, we describe the major mechanisms of damage, regeneration, and repair within the alveolar niche where gas exchange occurs. With a focus on viral infection, we summarize recent work that has established how epithelial proliferation is arrested during infection and how the innate immune system guides its reconstitution during recovery. The consequences of these processes going awry are also considered, with an emphasis on how this will impact postpandemic pulmonary biology and medicine.

中文翻译：

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风暴过后：病毒性肺损伤后肺泡上皮和先天免疫系统之间的再生、修复和稳态重建


哺乳动物的肺具有巨大的环境-上皮界面，该界面经过优化以完成呼吸系统的主要功能——气体交换。进化出如此大的表面积的后果之一是肺上皮不断暴露于毒素、刺激物和病原体。在这种环境中维持体内平衡需要上皮细胞和先天免疫系统之间的细胞信号传导达到微妙的平衡。损伤后，上皮可以在形式和功能上完全再生，也可以通过形成发育不良的疤痕组织进行修复。在这篇综述中，我们描述了发生气体交换的肺泡生态位内损伤、再生和修复的主要机制。我们重点关注病毒感染，总结了最近的工作，这些工作确定了感染期间如何阻止上皮增殖以及先天免疫系统如何在恢复期间指导其重建。还考虑了这些过程出错的后果，重点是这将如何影响大流行后的肺部生物学和医学。