ArticleMucosal immunology2015
ATG16L1 deficiency in macrophages drives clearance of uropathogenic E. coli in an IL-1β-dependent manner.
Article in Mucosal immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 81 citations in OpenAlex.
- Stress-Dependent NF-κB Signaling in Acute Kidney Injury: Linking Inflammation, Autophagy, and Apoptosis.International journal of molecular sciences · 2026Review
- A Scalable Organoid Model of Urothelial Aging for Metabolic Interrogation, Infection Modeling, and Reversal of Age-Associated Changes.Aging cell · 2026Article
- Emerging Nanomedicine Strategies for Sepsis: Immunomodulation and Beyond.Research (Washington, D.C.) · 2026Article
- Emerging Insights into the Interplay Between PANoptosis and Autophagy in Immune Regulation and Immune-Mediated Inflammatory Diseases.Medical sciences (Basel, Switzerland) · 2025Review
- PTEN modulates urinary tract infection susceptibility and shapes urothelial antibacterial defenses.Life science alliance · 2025Article
- Macrophage ATG16L1 promotes liver regeneration after partial hepatectomy.JHEP reports : innovation in hepatology · 2025Article
- EnterohemorrhagicAIMS microbiology · 2025Article
- The N-terminal domain ofFrontiers in immunology · 2025Article
- Fundamental and emerging insights into innate and adaptive immunity in inflammatory bowel diseases.Frontiers in immunology · 2025Review
- Autophagy and autophagic cell death in sepsis: friend or foe?Journal of intensive care · 2024Review
- Curcumin Attenuates Doxorubicin-Induced Cardiac Oxidative Stress and Increases Survival in Mice.Pharmaceutics · 2024Article
- The NLRP3 Inflammasome Is Dispensable in Methicillin-ResistantPathogens (Basel, Switzerland) · 2024Article
- D-Mannose reduces cellular senescence and NLRP3/GasderminD/IL-1β-driven pyroptotic uroepithelial cell shedding in the murine bladder.Developmental cell · 2024Article
- Molecular mechanisms of Sepsis attacking the immune system and solid organs.Frontiers in medicine · 2024Review
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- Trimethylamine N-Oxide (TMAO) Mediates Increased Inflammation and Colonization of Bladder Epithelial Cells during a UropathogenicPathogens (Basel, Switzerland) · 2023Article
- Effects of aging on urinary tract epithelial homeostasis and immunity.Developmental biology · 2023Review
- Sepsis-induced immunosuppression: mechanisms, diagnosis and current treatment options.Military Medical Research · 2022Review
- Alterations of autophagic and innate immune responses by the Crohn's disease-associatedWorld journal of gastroenterology · 2022Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Urinary tract infections (UTIs) are frequent, commonly recurrent, and costly. Deficiency in a key autophagy protein, ATG16L1, protects mice from infection with the predominant bacterial cause of UTIs, Uropathogenic E. coli (UPEC). Here, we report that loss of ATG16L1 in macrophages accounts for this protective phenotype. Compared with wild-type macrophages, macrophages deficient in ATG16L1 exhibit increased uptake of UPEC and enhanced secretion of interleukin-1β (IL-1β). The increased IL-1β production is dependent upon activation of the NLRP3 inflammasome and caspase-1. IL-1β secretion was also enhanced during UPEC infection of ATG16L1-deficient mice in vivo, and inhibition of IL-1β signaling abrogates the ATG16L1-dependent protection from UTIs. Our results argue that ATG16L1 normally suppresses a host-protective IL-1β response to UPEC by macrophages.
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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.