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Published on: May 4, 2016
Autophagy plays a protective role during Pseudomonas aeruginosa-induced apoptosis via ROS-MAPK pathway
Lu Han1,2, Qinmei Ma1,2, Jialin Yu1,2
1Key Laboratory of Ministry of Education for Protection and Utilization of Special Biological Resources in western China, NingXia University, NingXia, Yinchuan, China.
Abstract:
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.
Insights
Pseudomonas aeruginosa infection triggers apoptosis and autophagy in macrophages. Enhancing autophagy with rapamycin reduces cell death by lowering reactive oxygen species and impacting MAPK pathways.
Area of Science:
- Cellular biology
- Immunology
- Microbiology
Background:
- Pseudomonas aeruginosa infection induces alveolar macrophage apoptosis and autophagy, crucial for pathogen elimination.
- Autophagy and apoptosis are interconnected processes, but their interaction in P. aeruginosa infection is not fully understood.
- Investigating this interaction is vital for understanding host-pathogen dynamics.
Purpose of the Study:
- To explore the impact of P. aeruginosa infection on autophagy and apoptosis in RAW264.7 cells.
- To investigate the role of autophagy, stimulated by rapamycin, in P. aeruginosa-induced apoptosis.
- To elucidate the underlying molecular mechanisms, including reactive oxygen species (ROS) and MAPK pathways.
Main Methods:
- RAW264.7 cells were infected with P. aeruginosa.
- Autophagy was modulated using the activator rapamycin.
- Apoptosis, ROS levels, and MAPK pathway signaling (p-JNK, p-ERK1/2, p-p38) were assessed.
Main Results:
- P. aeruginosa infection induced both autophagy and apoptosis in RAW264.7 cells.
- Rapamycin treatment suppressed P. aeruginosa-induced apoptosis by regulating apoptosis-related proteins.
- Rapamycin reduced cellular ROS accumulation and diminished the activation of MAPK pathways.
Conclusions:
- Promoting autophagy via rapamycin attenuates P. aeruginosa-induced apoptosis in macrophages.
- Autophagy activation reduces ROS levels and impacts MAPK signaling, thereby protecting cells.
- These findings offer insights into host-pathogen interactions and suggest autophagy as a therapeutic target against P. aeruginosa infections.
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