Using TrkA KI mice and the derived primary pulmonary cells, in which the TrkA receptor tyrosine kinase activity can be specifically and effectively turned off by a small molecule 1NMPP1, we show in this study that the TrkA signaling is an important pathway to mediate both IAV replication and virus-induced airway inflammation, and that targeting TrkA signaling may provide an effective measure to protect against respiratory influenza disease. This evidence concerns the gene NTRK1 and inflammatory response.