Lu Han: Key Laboratory of Ministry of Education for Protection and Utilization of Special Biological Resources in western China, NingXia University, NingXia, Yinchuan, China.
Qinmei Ma: Key Laboratory of Ministry of Education for Protection and Utilization of Special Biological Resources in western China, NingXia University, NingXia, Yinchuan, China. ORCID
Jialin Yu: Key Laboratory of Ministry of Education for Protection and Utilization of Special Biological Resources in western China, NingXia University, NingXia, Yinchuan, China.
Zhaoqian Gong: Key Laboratory of Ministry of Education for Protection and Utilization of Special Biological Resources in western China, NingXia University, NingXia, Yinchuan, China.
Chenjie Ma: Key Laboratory of Ministry of Education for Protection and Utilization of Special Biological Resources in western China, NingXia University, NingXia, Yinchuan, China.
Yanan Xu: Key Laboratory of Ministry of Education for Protection and Utilization of Special Biological Resources in western China, NingXia University, NingXia, Yinchuan, China.
Guangcun Deng: Key Laboratory of Ministry of Education for Protection and Utilization of Special Biological Resources in western China, NingXia University, NingXia, Yinchuan, China.
Xiaoling Wu: Key Laboratory of Ministry of Education for Protection and Utilization of Special Biological Resources in western China, NingXia University, NingXia, Yinchuan, China. ORCID
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 -infected cell apoptosis is unclear. In this study, we explored the impact of 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 -infected RAW264.7 cells. The results indicated that infection induced autophagy and apoptosis in RAW264.7 cells, and that rapamycin could suppress -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 . In conclusion, the promotion of autophagy decreased -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 .
