Bacterial Manipulation of Autophagy Across Mammalian Cells and Psyllid Vectors: Conserved Strategies, Divergent Mechanisms, and Evidence Gaps

Autophagy restricts intracellular bacteria through xenophagy, yet many bacterial pathogens remodel this pathway to avoid degradation or support intracellular persistence. This review compares bacterial modulation of autophagy in mammalian cells and invertebrate vectors, with focusing on initiation, cargo recognition, autophagosome maturation, and autophagosome-lysosome fusion. In mammals, direct effector-host interactions have been defined for several pathogens. Legionella pneumophila RavZ effector removes lipidated ATG8/LC3 from autophagosome membranes. Salmonella typhimurium effectors interfere with AMPK-mTOR signaling, ATG16L1 recruitment, and Rab1A/TRAPPIII-dependent initiation. Shigella flexneri and Listeria monocytogenes mask bacterial surfaces to limit autophagic recognition. Mycobacterium tuberculosis, Anaplasma phagocytophilum, Staphylococcus aureus, and Coxiella burnetii exploit autophagy-related compartments while restricting degradative maturation. In invertebrate systems, especially psyllid vectors of Candidatus Liberibacter asiaticus and Candidatus Liberibacter solanacearum, current evidence indicates pathogen-associated changes in ATG gene expression, endoplasmic reticulum-associated vacuole formation, calcium and ROS signaling, lysosomal activity, and vitellogenin-linked regulation. However, these mechanisms are supported mainly by transcriptomic, microscopy-based, pharmacological, and protein-interaction evidence, and direct effector-mediated control of psyllid autophagy remains insufficiently demonstrated. We propose that bacterial control of autophagy follows conserved logic across host systems. This logic includes suppression of xenophagic recognition, remodeling of autophagosome biogenesis, and uncoupling of autophagosome formation from lysosomal dagradation. Defining which mechanisms are directly effector-driven and which are host-response signatures will be essential for translating autophagy biology into antimicrobial, vector-control, and plant disease-management strategies.