Autophagy in Pseudomonas aeruginosa infection: host defense, bacterial countermeasures, and therapeutic targeting
4 affiliations
- 1The Fourth Clinical Medical College of Guangzhou University of Chinese Medicine, Shenzhen, China
- 2Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, China
- 3Shenzhen Hospital of Integrated Traditional Chinese and Western Medicine, Shenzhen, China
- 4School of Chinese Medicine, The University of Hong Kong, Pok Fu Lam, Hong Kong SAR, China
Abstract
Pseudomonas aeruginosa (P. aeruginosa) is a major opportunistic pathogen whose diverse virulence strategies, increasing antibiotic resistance, and ability to establish persistent infections continue to compromise the efficacy of conventional antimicrobial therapies. Although traditionally regarded as an extracellular pathogen, P. aeruginosa can also enter and persist within host cells, triggering inflammatory responses and cellular injury while simultaneously modulating host autophagic responses. On the one hand, xenophagy and related autophagic processes recognize and deliver intracellular bacteria for lysosomal degradation. Mitophagy eliminates damaged mitochondria generated during infection and limits the accumulation of mitochondrial danger signals. Meanwhile, autophagy regulates inflammasome activation by controlling the removal of damaged organelles and inflammasome components, thereby shaping inflammatory responses during infection. Collectively, these processes contribute to the protective role of autophagy in host defense against P. aeruginosa infection. On the other hand, P. aeruginosa can interfere with or remodel host autophagy through secreted effector molecules, quorum sensing signals, and infection-induced host signaling pathways, resulting in a functional disconnect between autophagic activation and effective bacterial clearance or other antimicrobial responses. This review summarizes current advances in understanding the interplay between autophagy and P. aeruginosa, highlighting the protective functions of autophagy in host defense, the countermeasures employed by P. aeruginosa to evade autophagic clearance, and the therapeutic implications of these host–pathogen interactions. These insights may support the development of host-directed therapeutic approaches targeting autophagy to improve antibacterial defense against P. aeruginosa.
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BibTeX
@article{zhang2026autophagy,
title = {{Autophagy in Pseudomonas aeruginosa infection: host defense, bacterial countermeasures, and therapeutic targeting}},
author = {Bingbing Zhang and Yanling Huang and Lingling Wen and Qiaoli Hua and Lijun Zhao and Jiangang Shen and Meiling Zhu},
journal = {Frontiers in Microbiology},
year = {2026},
month = oct,
doi = {10.3389/fmicb.2026.1976209},
url = {https://doi.org/10.3389/fmicb.2026.1976209},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Autophagy in Pseudomonas aeruginosa infection: host defense, bacterial countermeasures, and therapeutic targeting
AU - Bingbing Zhang
AU - Yanling Huang
AU - Lingling Wen
AU - Qiaoli Hua
AU - Lijun Zhao
AU - Jiangang Shen
AU - Meiling Zhu
PY - 2026
DA - 2026/10/12
JO - Frontiers in Microbiology
DO - 10.3389/fmicb.2026.1976209
UR - https://doi.org/10.3389/fmicb.2026.1976209
AB - Pseudomonas aeruginosa (P. aeruginosa) is a major opportunistic pathogen whose diverse virulence strategies, increasing antibiotic resistance, and ability to establish persistent infections continue to compromise the efficacy of conventional antimicrobial therapies. Although traditionally regarded as an extracellular pathogen, P. aeruginosa can also enter and persist within host cells, triggering inflammatory responses and cellular injury while simultaneously modulating host autophagic responses. On the one hand, xenophagy and related autophagic processes recognize and deliver intracellular bacteria for lysosomal degradation. Mitophagy eliminates damaged mitochondria generated during infection and limits the accumulation of mitochondrial danger signals. Meanwhile, autophagy regulates inflammasome activation by controlling the removal of damaged organelles and inflammasome components, thereby shaping inflammatory responses during infection. Collectively, these processes contribute to the protective role of autophagy in host defense against P. aeruginosa infection. On the other hand, P. aeruginosa can interfere with or remodel host autophagy through secreted effector molecules, quorum sensing signals, and infection-induced host signaling pathways, resulting in a functional disconnect between autophagic activation and effective bacterial clearance or other antimicrobial responses. This review summarizes current advances in understanding the interplay between autophagy and P. aeruginosa, highlighting the protective functions of autophagy in host defense, the countermeasures employed by P. aeruginosa to evade autophagic clearance, and the therapeutic implications of these host–pathogen interactions. These insights may support the development of host-directed therapeutic approaches targeting autophagy to improve antibacterial defense against P. aeruginosa.
SN - 1664-302X
ER -