Weill Cornell Medicine, Division of Pulmonary and Critical Care, New York, NY 10021, USA.
Int J Mol Sci. 2021 Nov 9;22(22):12097. doi: 10.3390/ijms222212097.
Influenza is a respiratory virus that alone or in combination with secondary bacterial pathogens can contribute to the development of acute pneumonia in persons >65 years of age. Host innate immune antiviral signaling early in response to influenza is essential to inhibit early viral replication and guide the initiation of adaptive immune responses. Using young adult (3 months) and aged adult mice infected with mouse adapted H1N1 or H3N2, the results of our study illustrate dysregulated and/or diminished activation of key signaling pathways in aged lung contribute to increased lung inflammation and morbidity. Specifically, within the first seven days of infection, there were significant changes in genes associated with TLR and RIG-I signaling detected in aged murine lung in response to H1N1 or H3N2. Taken together, the results of our study expand our current understanding of age-associated changes in antiviral signaling in the lung.
流感是一种呼吸道病毒，它可以单独或与继发性细菌病原体一起导致 >65 岁人群发生急性肺炎。宿主对流感的先天抗病毒信号转导在早期抑制病毒复制和指导适应性免疫反应的启动中至关重要。本研究使用感染了经小鼠适应的 H1N1 或 H3N2 的年轻成年（3 个月）和老年成年小鼠，结果表明，老年肺部关键信号通路的失调和/或减弱激活导致肺部炎症和发病率增加。具体而言，在感染后的头 7 天内，H1N1 或 H3N2 感染后老年小鼠肺部与 TLR 和 RIG-I 信号转导相关的基因发生了显著变化。总之，我们的研究结果扩展了我们对肺部抗病毒信号转导中与年龄相关变化的现有认识。
