ArticleJournal of immunology (Baltimore, Md. : 1950)2009
Neisseria gonorrhoeae activates the proteinase cathepsin B to mediate the signaling activities of the NLRP3 and ASC-containing inflammasome.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 165 papers.
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Who cites it
165 citing papers in PubMed, 266 citations in OpenAlex.
- Differential Host Gene Expression Associated with Non-Research square · 2026Article
- Cinnamaldehyde inhibits the NLRP3 inflammasome and inflammatory response by reducing oxidative stress in Neisseria gonorrhoeae-infected macrophages.Journal of traditional and complementary medicine · 2026Article
- MtrR Regulates a Major Lytic Transglycosylase (Microorganisms · 2026Article
- AI-driven insights into protein misfolding and innate immunity in neurodegenerative diseases.Frontiers in immunology · 2026Review
- Effects of surface-exposed sialic acid and LOS outer core on the ability of native Neisseria meningitidis outer membrane vesicles (nOMVs) to induce cytokine expression and pyroptotic pathways in THP-1-derived macrophages.Scientific reports · 2025Article
- Molecular mechanisms and regulation of inflammasome activation and signaling: sensing of pathogens and damage molecular patterns.Cellular & molecular immunology · 2025Review
- Computational modeling approach to identify potential anti-Campylobacter peptides fromOpen veterinary journal · 2025Review
- Loss of Type 2 Bone Morphogenetic Protein Receptor Activates NOD-Like Receptor Family Protein 3/Gasdermin E-Mediated Pyroptosis in Pulmonary Arterial Hypertension.Journal of the American Heart Association · 2025Article
- The Ambiguous Role of HMGB1 Across the Hallmarks of Aging: A Narrative Review.Clinical interventions in aging · 2025Review
- NLRP3 Inflammasome in Gynecologic Inflammatory Diseases: Mechanisms, Pathophysiology, and Therapeutic Strategies.Journal of inflammation research · 2025Review
- The Role of NLRP3 Inflammasome in Oral Squamous Cell Carcinoma.Journal of inflammation research · 2025Review
- Review
- The interplay of transition metals in ferroptosis and pyroptosis.Cell division · 2024Review
- Targeting TANK-binding kinase 1 attenuates painful diabetic neuropathy via inhibiting microglia pyroptosis.Cell communication and signaling : CCS · 2024Article
- Vaginal microbes alter epithelial transcriptome and induce epigenomic modifications providing insight into mechanisms for susceptibility to adverse reproductive outcomes.Research square · 2024Article
- IL-17C is a driver of damaging inflammation during Neisseria gonorrhoeae infection of human Fallopian tube.Nature communications · 2024Article
- Biomaterials Functionalized with Inflammasome Inhibitors-Premises and Perspectives.Journal of functional biomaterials · 2024Review
- Honokiol Exhibits Anti-NLRP3 Inflammasome and Antimicrobial Properties inJournal of inflammation research · 2024Article
- Inflammasome signalling pathway in the regulation of inflammation - its involvement in the development and exacerbation of asthma and chronic obstructive pulmonary disease.Postepy dermatologii i alergologii · 2023Review
- Bacterium of one thousand and one variants: genetic diversity ofMicrobial genomics · 2023Review
105 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
Neisseria gonorrhoeae is a common sexually transmitted pathogen that significantly impacts female fertility, neonatal health, and transmission of HIV worldwide. N. gonorrhoeae usually causes localized inflammation of the urethra and cervix by inducing production of IL-1beta and other inflammatory cytokines. Several NLR (nucleotide-binding domain, leucine-rich repeat) proteins are implicated in the formation of pro-IL-1beta-processing complexes called inflammasomes in response to pathogens. We demonstrate that NLRP3 (cryopyrin, NALP3) is the primary NLR required for IL-1beta/IL-18 secretion in response to N. gonorrhoeae in monocytes. We also show that N. gonorrhoeae infection promotes NLRP3-dependent monocytic cell death via pyronecrosis, a recently described pathway with morphological features of necrosis, including release of the strong inflammatory mediator HMBG1. Additionally, N. gonorrhoeae activates the cysteine protease cathepsin B as measured by the breakdown of a cathepsin B substrate. Inhibition of cathepsin B shows that this protease is an apical controlling step in the downstream activities of NLRP3 including IL-1beta production, pyronecrosis, and HMGB1 release. Nonpathogenic Neisseria strains (Neisseria cinerea and Neisseria flavescens) do not activate NLRP3 as robustly as N. gonorrhoeae. Conditioned medium from N. gonorrhoeae contains factors capable of initiating the NLRP3-mediated signaling events. Isolated N. gonorrhoeae lipooligosaccharide, a known virulence factor from this bacterium that is elaborated from the bacterium in the form of outer membrane blebs, activates both NLRP3-induced IL-1beta secretion and pyronecrosis. Our findings indicate that activation of NLRP3-mediated inflammatory response pathways is an important venue associated with host response and pathogenesis of N. gonorrhoeae.
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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.