ArticlePLoS pathogens2023
Neisseria gonorrhoeae co-opts C4b-binding protein to enhance complement-independent survival from neutrophils.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 16 citations in OpenAlex.
- C4BP occludes the non-opsonic interaction ofInfection and immunity · 2026Article
- C4BP occludes the non-opsonic interaction ofbioRxiv : the preprint server for biology · 2026Article
- Review
- Pre-clinical efficacy of a C4BP hexameric IgG Fc fusion protein against Neisseria gonorrhoeae.PloS one · 2026Article
- Neutrophil CEACAMs and the Inflammatory Response toJournal of innate immunity · 2026Review
- Identification of a Kingella kingae factor H binding protein that is the major determinant of serum resistance.PLoS pathogens · 2025Article
- Terminal complement complexes with or without C9 potentiate antimicrobial activity againstmBio · 2025Article
- Rethinking concepts of virulence with Neisseria gonorrhoeae.Nature microbiology · 2025Article
- Article
- Addressing Sexually Transmitted Infections Due toMicroorganisms · 2024Review
- Gonococcal PorB: a multifaceted modulator of host immune responses.Trends in microbiology · 2024Review
- Proteomics Clustering Research of ITRAQ Markers in Plasma of AIDS Patients with Different Chinese Medicine Syndromes.Iranian journal of public health · 2024Article
- Article
- Evaluating vaccine-elicited antibody activities againstInfection and immunity · 2023Article
- Diverse Functions of C4b-Binding Protein in Health and Disease.Journal of immunology (Baltimore, Md. : 1950) · 2023Review
- Immune responses toFrontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Neisseria gonorrhoeae (Gc) is a human-specific pathogen that causes the sexually transmitted infection gonorrhea. Gc survives in neutrophil-rich gonorrheal secretions, and recovered bacteria predominantly express phase-variable, surface-expressed opacity-associated (Opa) proteins (Opa+). However, expression of Opa proteins like OpaD decreases Gc survival when exposed to human neutrophils ex vivo. Here, we made the unexpected observation that incubation with normal human serum, which is found in inflamed mucosal secretions, enhances survival of Opa+ Gc from primary human neutrophils. We directly linked this phenomenon to a novel complement-independent function for C4b-binding protein (C4BP). When bound to the bacteria, C4BP was necessary and sufficient to suppress Gc-induced neutrophil reactive oxygen species production and prevent neutrophil phagocytosis of Opa+ Gc. This research identifies for the first time a complement-independent role for C4BP in enhancing the survival of a pathogenic bacterium from phagocytes, thereby revealing how Gc exploits inflammatory conditions to persist at human mucosal surfaces.
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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.