ArticleScientific reports2020
α-Hemolysin of uropathogenic E. coli regulates NLRP3 inflammasome activation and mitochondrial dysfunction in THP-1 macrophages.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Prevalence of bovine endometritis, virulence mechanisms ofVirulence · 2026Pooled it
- Gut microbiota dysbiosis exacerbates acute pancreatitis viaGut microbes · 2026Article
- Mechanisms Linking Recurrent Bacterial Urinary Tract Infections to Chronic Kidney Disease Progression.International journal of molecular sciences · 2026Review
- Sulfonamide resistance, virulence traits, and in-silico target interactions among clinical isolates in Setif, Algeria (2021-2023).Iranian journal of microbiology · 2025Article
- LDL receptor-mediated endocytosis ofProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Vibrio cholerae cytolysin induces pro-inflammatory and death signals through novel TLR assembly.PLoS pathogens · 2025Article
- PANoptosis in Bacterial Infections: A Double-Edged Sword Balancing Host Immunity and Pathogenesis.Pathogens (Basel, Switzerland) · 2025Review
- Synthetic antimicrobial peptide LD4-PP protects the host againstFrontiers in immunology · 2025Article
- Article
- Uropathogen and host responses in pyelonephritis.Nature reviews. Nephrology · 2023Review
- Inflammasome pathway in kidney transplantation.Frontiers in medicine · 2023Review
- A detailed molecular network map and model of the NLRP3 inflammasome.Frontiers in immunology · 2023Review
- Nucleotide receptors mediate protection against neonatal sepsis and meningitis caused by alpha-hemolysin expressing Escherichia coli K1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Bacterial pore-forming toxins.Microbiology (Reading, England) · 2022Article
- Review
- The Direct Semi-Quantitative Detection of 18 Pathogens and Simultaneous Screening for Nine Resistance Genes in Clinical Urine Samples by a High-Throughput Multiplex Genetic Detection System.Frontiers in cellular and infection microbiology · 2021Article
- Dihydrotanshinone I Specifically Inhibits NLRP3 Inflammasome Activation and Protects Against Septic ShockFrontiers in pharmacology · 2021Article
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hemolysin expressing UPEC strains have been associated with severe advanced kidney pathologies, such as cystitis and pyelonephritis, which are associated with an inflammatory response. Macrophages play an important role in regulating an inflammatory response during a urinary tract infection. We have studied the role of purified recombinant α-hemolysin in inducing inflammatory responses and cell death in macrophages. Acylation at lysine residues through HlyC is known to activate proHlyA into a fully functional pore-forming toxin, HlyA. It was observed that active α-hemolysin (HlyA) induced cleavage of caspase-1 leading to the maturation of IL-1β, while inactive α-hemolysin (proHlyA) failed to do so in THP-1 derived macrophages. HlyA also promotes deubiquitination, oligomerization, and activation of the NLRP3 inflammasome, which was found to be dependent on potassium efflux. We have also observed the co-localization of NLRP3 within mitochondria during HlyA stimulations. Moreover, blocking of potassium efflux improved the mitochondrial health in addition to a decreased inflammatory response. Our study demonstrates that HlyA stimulation caused perturbance in potassium homeostasis, which led to the mitochondrial dysfunction followed by an acute inflammatory response, resulting in cell death. However, the repletion of intracellular potassium stores could avoid HlyA induced macrophage cell death. The findings of this study will help to understand the mechanism of α-hemolysin induced inflammatory response and cell death.
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