ArticleThe Journal of infectious diseases2024
Uropathogenic Escherichia coli Subverts Host Autophagic Defenses by Stalling Preautophagosomal Structures to Escape Lysosome Exocytosis.
Article in The Journal of infectious diseases, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Role of bacterial outer membrane vesicles in immune evasion during infection.Archives of microbiology · 2026Review
- Urinary Tract Infections: Molecular Determinants of Uropathogenicity and Their Translation into Contemporary Clinical Practice.International journal of molecular sciences · 2026Review
- Targeted lysosomal activation in bladder epithelium enhances clearance of intracellular uropathogenic Escherichia coli.PLoS pathogens · 2026Article
- Decoding epithelial-immune cell crosstalk in uropathogenicFrontiers in microbiology · 2026Review
- Progranulin inhibits autophagy to facilitate intracellular colonization ofFrontiers in cellular and infection microbiology · 2024Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Urinary tract infections are primarily caused by uropathogenic Escherichia coli (UPEC). UPEC infects bladder epithelial cells (BECs) via fusiform vesicles and escapes into the cytosol by disrupting fusiform vesicle membrane using outer membrane phospholipase PldA, and establishes biofilm-like intracellular bacterial communities (IBCs) for protection from host immune clearance. Cytosolic UPEC is captured by autophagy to form autophagosomes, then transported to lysosomes, triggering the spontaneous exocytosis of lysosomes. The mechanism by which UPEC evades autophagy to recognize and form IBCs remains unclear. Here, we demonstrate that by inhibiting autophagic flux, UPEC PldA reduces the lysosome exocytosis of BECs. By reducing intracellular phosphatidylinositol 3-phosphate levels, UPEC PldA increases the accumulation of NDP52 granules and decreases the targeting of NDP52 to autophagy, hence stalling preautophagosome structures. Thus, our results uncover a critical role for PldA to inhibit autophagic flux, favoring UPEC escapes from lysosome exocytosis, thereby contributing to acute urinary tract infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.