Pseudomonas aeruginosa infection can induce alveolar macrophage apoptosis and autophagy, which play a vital role in eliminating pathogens. These two processes are usually not independent. Recently, autophagy has been found to interact with apoptosis during pathogen infections. Nevertheless, the role of autophagy in P. aeruginosa-infected cell apoptosis is unclear. In this study, we explored the impact of P. aeruginosa infection on autophagy and apoptosis in RAW264.7 cells. The autophagy activator rapamycin was used to stimulate autophagy and explore the role of autophagy on apoptosis in P. aeruginosa-infected RAW264.7 cells. The results indicated that P. aeruginosa infection induced autophagy and apoptosis in RAW264.7 cells, and that rapamycin could suppress P. aeruginosa-induced apoptosis by regulating the expression of apoptosis-related proteins. In addition, rapamycin scavenged the cellular reactive oxygen species (ROS) and diminished p-JNK, p-ERK1/2 and p-p38 expression of MAPK pathways in RAW264.7 cells infected with P. aeruginosa. In conclusion, the promotion of autophagy decreased P. aeruginosa-induced ROS accumulation and further attenuated the apoptosis of RAW264.7 cells through MAPK pathway. These results provide novel insights into host–pathogen interactions and highlight a potential role of autophagy in eliminating P. aeruginosa.

铜绿假单胞菌感染可诱导肺泡巨噬细胞凋亡和自噬，对清除病原体起着至关重要的作用。这两个过程通常不是独立的。最近，发现自噬在病原体感染期间与细胞凋亡相互作用。然而，自噬在铜绿假单胞菌感染的细胞凋亡中的作用尚不清楚。在本研究中，我们探讨了铜绿假单胞菌感染对RAW264.7细胞自噬和凋亡的影响。采用自噬激活剂雷帕霉素刺激自噬，探讨自噬对铜绿假单胞菌感染的RAW264.7细胞凋亡的作用。结果表明，铜绿假单胞菌感染诱导RAW264.7细胞发生自噬和凋亡，雷帕霉素可以通过调节凋亡相关蛋白的表达来抑制铜绿假单胞菌诱导的细胞凋亡。此外，雷帕霉素清除感染铜绿假单胞菌的RAW264.7细胞中的细胞活性氧（ROS）并减少MAPK途径的p-JNK、p-ERK1/2和p-p38表达。总之，自噬的促进减少了铜绿假单胞菌诱导的ROS积累，并通过MAPK途径进一步减弱了RAW264.7细胞的凋亡。这些结果为宿主与病原体相互作用提供了新的见解，并强调了自噬在消除铜绿假单胞菌中的潜在作用。