Since the twentieth century, four influenza pandemics caused by IAV have killed millions of people worldwide. IAV infection could induce acute lung injury mediated by cytokine storms, which is an essential cause of death in critically ill patients. Consequently, it is crucial to explore the regulators and regulatory mechanisms of cytokine storms, which may provide potential drug targets and expand our understanding of acute lung injury. Previous studies have shown that JNK kinase is essential in promoting inflammatory responses during viral infections. In this study, we demonstrated that JNK kinase could regulate the IAV-induced cytokine storms by affecting the expression of pro-inflammatory and anti-inflammatory factors. Further studies revealed that inhibition of JNK kinase activity significantly downregulated the expression of the inflammatory amplifier TREM1. Besides, TREM1 knockdown could significantly inhibit the expression of pro-inflammatory factors. Furthermore, SP600125 is a specific inhibitor of JNK kinase. The results show that TREM1 overexpression reversed the effect of SP600125 treatment on the expression of pro-inflammatory factors. Together, we found that JNK kinase could activate the inflammatory amplifier TREM1 to promote inflammatory responses during influenza A virus infection. These findings may provide some inspiration for subsequent researchers to explore the regulatory mechanisms of cytokine storms induced by emerging viral infections.