Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Cell Tissue Res. 2011 Jan;343(1):13-21. doi: 10.1007/s00441-010-1043-z. Epub 2010 Sep 17.
Infection by influenza virus leads to respiratory failure characterized by acute lung injury associated with alveolar edema, necrotizing bronchiolitis, and excessive bleeding. Severe reactions to infection that lead to hospitalizations and/or death are frequently attributed to an exuberant host response, with excessive inflammation and damage to the epithelial cells that mediate respiratory gas exchange. The respiratory mucosa serves as a physical and chemical barrier to infection, producing mucus and surfactants, anti-viral mediators, and inflammatory cytokines. The airway epithelial cell layer also serves as the first and overwhelmingly primary target for virus infection and growth. This review details immune events during influenza infection from the viewpoint of the epithelial cells, secretory host defense mechanisms, cell death, and recovery.
流感病毒感染可导致呼吸衰竭，其特征是急性肺损伤与肺泡水肿、坏死性细支气管炎和过度出血有关。导致住院和/或死亡的严重感染反应通常归因于过度的宿主反应，导致上皮细胞过度炎症和损伤，从而影响呼吸气体交换。呼吸道黏膜作为感染的物理和化学屏障，可产生黏液和表面活性剂、抗病毒介质和炎症细胞因子。气道上皮细胞层也是病毒感染和生长的第一且绝对主要靶标。这篇综述从上皮细胞的角度详细描述了流感感染期间的免疫事件、分泌型宿主防御机制、细胞死亡和恢复。
