Pediatric Intensive Care Unit, Emma Children's Hospital, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands.
Viruses. 2013 Jan 23;5(1):406-22. doi: 10.3390/v5010406.
Pneumovirus infections cause a wide spectrum of respiratory disease in humans and animals. The airway epithelium is the major site of pneumovirus replication. Apoptosis or regulated cell death, may contribute to the host anti-viral response by limiting viral replication. However, apoptosis of lung epithelial cells may also exacerbate lung injury, depending on the extent, the timing and specific location in the lungs. Differential apoptotic responses of epithelial cells versus innate immune cells (e.g., neutrophils, macrophages) during pneumovirus infection can further contribute to the complex and delicate balance between host defense and disease pathogenesis. The purpose of this manuscript is to give an overview of the role of apoptosis in pneumovirus infection. We will examine clinical and experimental data concerning the various pro-apoptotic stimuli and the roles of apoptotic epithelial and innate immune cells during pneumovirus disease. Finally, we will discuss potential therapeutic interventions targeting apoptosis in the lungs.
呼吸道合胞病毒感染可引起人类和动物广泛的呼吸道疾病。气道上皮细胞是呼吸道合胞病毒复制的主要部位。细胞凋亡或程序性细胞死亡,通过限制病毒复制,可能有助于宿主抗病毒反应。然而,肺上皮细胞的凋亡也可能加重肺部损伤,这取决于损伤的程度、时间和在肺部的具体位置。呼吸道合胞病毒感染过程中上皮细胞与固有免疫细胞(如中性粒细胞、巨噬细胞)的凋亡反应差异,可进一步影响宿主防御和疾病发病机制之间的复杂微妙平衡。本文旨在概述细胞凋亡在呼吸道合胞病毒感染中的作用。我们将检查有关各种促凋亡刺激物的临床和实验数据,以及凋亡上皮细胞和固有免疫细胞在呼吸道合胞病毒疾病中的作用。最后,我们将讨论针对肺部细胞凋亡的潜在治疗干预措施。