The impact of influenza pulmonary infection and inflammation on vagal bronchopulmonary sensory neurons

Influenza A virus (IAV) is rapidly detected in the airways by the immune system, with resident parenchymal cells and leukocytes orchestrating viral sensing and the induction of antiviral inflammatory responses. The airways are innervated by heterogenous populations of vagal sensory neurons which also play an important role in pulmonary defense. How these neurons respond to IAV respiratory infection remains unclear. Here, we use a murine model to provide the first evidence that vagal sensory neurons undergo significant transcriptional changes following a respiratory IAV infection. RNA sequencing on vagal sensory ganglia showed that IAV infection induced the expression of many genes associated with an antiviral and pro-inflammatory response Transcriptome of vagal sensory ganglia obtained from mice infected with a respiratory pathogen (influenza A)

甲型流感病毒（Influenza A virus, IAV）可被气道内的免疫系统快速识别，固有实质细胞与白细胞协同介导病毒感知，并启动抗病毒炎症应答。气道由异质性迷走感觉神经元群支配，此类神经元在肺部防御中同样发挥关键作用。目前尚不明确这类神经元如何应对甲型流感病毒的呼吸道感染。本研究借助小鼠模型，首次证实迷走感觉神经元在呼吸道甲型流感病毒感染后会发生显著的转录组改变。对迷走感觉神经节的RNA测序结果显示，甲型流感病毒感染可诱导大量与抗病毒及促炎应答相关的基因表达。本数据集为取自感染呼吸道病原体（甲型流感病毒）小鼠的迷走感觉神经节转录组。