ArticleProceedings of the National Academy of Sciences of the United States of America2012
Atg16L1 deficiency confers protection from uropathogenic Escherichia coli infection in vivo.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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71 citing papers in PubMed, 97 citations in OpenAlex.
- Nanogels conjugated with cell-penetrating peptide as drug delivery vehicle for treating urinary tract infections.Nanomedicine : nanotechnology, biology, and medicine · 2025Article
- The N-terminal domain ofFrontiers in immunology · 2025Article
- Nur77 protects the bladder urothelium from intracellular bacterial infection.Nature communications · 2024Article
- Uropathogenic Escherichia coli Subverts Host Autophagic Defenses by Stalling Preautophagosomal Structures to Escape Lysosome Exocytosis.The Journal of infectious diseases · 2024Article
- D-Mannose reduces cellular senescence and NLRP3/GasderminD/IL-1β-driven pyroptotic uroepithelial cell shedding in the murine bladder.Developmental cell · 2024Article
- Bladder-draining lymph nodes support germinal center B cell responses during urinary tract infection in mice.Infection and immunity · 2023Article
- Supraphysiologic Vaginal Estrogen Therapy in Aged Mice Mitigates Age-Associated Bladder Inflammatory Response to Urinary Tract Infections.Urogynecology (Philadelphia, Pa.) · 2023Article
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- Entamoeba histolytica exploits the autophagy pathway in macrophages to trigger inflammation in disease pathogenesis.Mucosal immunology · 2021Article
- Molecular determinants of disease severity in urinary tract infection.Nature reviews. Urology · 2021Review
- An infection-induced RhoB-Beclin 1-Hsp90 complex enhances clearance of uropathogenic Escherichia coli.Nature communications · 2021Article
- Crohn's disease-associated ATG16L1 T300A genotype is associated with improved survival in gastric cancer.EBioMedicine · 2021Article
- Autophagy-A Story of Bacteria Interfering with the Host Cell Degradation Machinery.Pathogens (Basel, Switzerland) · 2021Review
- Autophagy Inhibition Enables Nrf2 to Exaggerate the Progression of Diabetic Cardiomyopathy in Mice.Diabetes · 2020Article
- The immune response to infection in the bladder.Nature reviews. Urology · 2020Review
- Autophagy and microbial pathogenesis.Cell death and differentiation · 2020Review
- Autophagy in neutrophils.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2020Review
- Cyclooxygenase-2 Inhibition Reduces Autophagy of Macrophages Enhancing Extraintestinal PathogenicFrontiers in microbiology · 2020Article
- Autophagy-mediated regulation of neutrophils and clinical applications.Burns & trauma · 2020Review
11 more citing papers are in PubMed but not listed here.
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7 authors at 3 institutions in 2 countries.
Funding
Abstract
Urinary tract infection (UTI), a frequent and important disease in humans, is primarily caused by uropathogenic Escherichia coli (UPEC). UPEC forms acute cytoplasmic biofilms within superficial urothelial cells and can persist by establishing membrane-enclosed latent reservoirs to seed recurrent UTI. The host responds with an influx of innate immune cells and shedding of infected epithelial cells. The autophagy gene ATG16L1 has a commonly occurring mutation that is associated with inflammatory disease and intestinal cell abnormalities in mice and humans. Here, we show that Atg16L1-deficient mice (Atg16L1(HM)) cleared bacteriuria more rapidly and thoroughly than controls and showed rapid epithelial recovery. Atg16L1 deficiency was associated with a potent proinflammatory cytokine response with increased recruitment of monocytes and neutrophils to infected bladders. Chimeric and genetic studies showed that Atg16L1(HM) hematopoietic cells alone could increase clearance and that Atg16L1-deficient innate immune cells were required and sufficient for enhanced bacteriuric clearance. We also show that Atg16L1-deficient mice exhibit cell-autonomous architectural aberrations of superficial urothelial cells, including increases in multivesicular bodies, lysosomes, and expression of the UPEC receptor Up1a. Finally, we show that Atg16L1(HM) epithelial cells contained a significantly reduced number of latent reservoirs. Together, our results show that Atg16L1 deficiency confers protection in vivo to the host against both acute and latent UPEC infection, suggest that deficiency in a key autophagy protein can be protective against infection in an animal model of one of the most common diseases of women worldwide, and may have significant clinical implications for understanding the etiology of recurrent UTIs.
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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.