ArticleMucosal immunology2016
Strain- and host species-specific inflammasome activation, IL-1β release, and cell death in macrophages infected with uropathogenic Escherichia coli.
Article in Mucosal immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 82 citations in OpenAlex.
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- Dopamine-driven increase in IL-1β in myeloid cells is mediated by differential dopamine receptor expression and exacerbated by HIV.Journal of neuroinflammation · 2025Article
- Gasdermin D in macrophages drives orchitis by regulating inflammation and antigen presentation processes.EMBO molecular medicine · 2024Article
- The NLRP3 Inflammasome Is Dispensable in Methicillin-ResistantPathogens (Basel, Switzerland) · 2024Article
- P2X7 receptor activation leads to NLRP3-independent IL-1β release by human macrophages.Cell communication and signaling : CCS · 2023Article
- Bladder-draining lymph nodes support germinal center B cell responses during urinary tract infection in mice.Infection and immunity · 2023Article
- A human urothelial microtissue model reveals shared colonization and survival strategies between uropathogens and commensals.Science advances · 2023Article
- Engineer a double team of short-lived and glucose-sensing bacteria for cancer eradication.Cell reports. Medicine · 2023Article
- Human neutrophil peptides 1-3 protect the murine urinary tract from uropathogenicProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Immunomodulation therapy offers new molecular strategies to treat UTI.Nature reviews. Urology · 2022Review
- Timing is everything: impact of development, ageing and circadian rhythm on macrophage functions in urinary tract infections.Mucosal immunology · 2022Review
- Dec2 inhibits macrophage pyroptosis to promote periodontal homeostasis.Journal of periodontal & implant science · 2022Article
- Modified horseshoe crab peptides target and kill bacteria inside host cells.Cellular and molecular life sciences : CMLS · 2021Article
- Article
- From pyroptosis, apoptosis and necroptosis to PANoptosis: A mechanistic compendium of programmed cell death pathways.Computational and structural biotechnology journal · 2021Review
- Oxalate Alters Cellular Bioenergetics, Redox Homeostasis, Antibacterial Response, and Immune Response in Macrophages.Frontiers in immunology · 2021Article
- HIV Neuropathogenesis in the Presence of a Disrupted Dopamine System.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020Review
- Functionally distinct resident macrophage subsets differentially shape responses to infection in the bladder.Science advances · 2020Article
- α-Hemolysin of uropathogenic E. coli regulates NLRP3 inflammasome activation and mitochondrial dysfunction in THP-1 macrophages.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Uropathogenic Escherichia coli (UPEC) is the main etiological agent of urinary tract infections (UTIs). Little is known about interactions between UPEC and the inflammasome, a key innate immune pathway. Here we show that UPEC strains CFT073 and UTI89 trigger inflammasome activation and lytic cell death in human macrophages. Several other UPEC strains, including two multidrug-resistant ST131 isolates, did not kill macrophages. In mouse macrophages, UTI89 triggered cell death only at a high multiplicity of infection, and CFT073-mediated inflammasome responses were completely NLRP3-dependent. Surprisingly, CFT073- and UTI89-mediated responses only partially depended on NLRP3 in human macrophages. In these cells, NLRP3 was required for interleukin-1β (IL-1β) maturation, but contributed only marginally to cell death. Similarly, caspase-1 inhibition did not block cell death in human macrophages. In keeping with such differences, the pore-forming toxin α-hemolysin mediated a substantial proportion of CFT073-triggered IL-1β secretion in mouse but not human macrophages. There was also a more substantial α-hemolysin-independent cell death response in human vs. mouse macrophages. Thus, in mouse macrophages, CFT073-triggered inflammasome responses are completely NLRP3-dependent, and largely α-hemolysin-dependent. In contrast, UPEC activates an NLRP3-independent cell death pathway and an α-hemolysin-independent IL-1β secretion pathway in human macrophages. This has important implications for understanding UTI in humans.
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