ArticlePLoS pathogens2014
Global analysis of neutrophil responses to Neisseria gonorrhoeae reveals a self-propagating inflammatory program.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 56 citations in OpenAlex.
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- Neutrophil CEACAMs and the Inflammatory Response toJournal of innate immunity · 2026Review
- Flavin affinity for the reductase HpaC differentially sensitizes Neisseria gonorrhoeae during Type IV pilus-dependent killing.PLoS pathogens · 2025Article
- Meningococcal vaccine 4CMenB elicits a robust cellular immune response that targets but is not consistently protective againstmSphere · 2025Article
- The role of CEACAMs in neutrophil function.European journal of clinical investigation · 2024Review
- Dual species transcriptomics reveals conserved metabolic and immunologic processes in interactions between human neutrophils and Neisseria gonorrhoeae.PLoS pathogens · 2024Article
- Article
- Vertebrate and Invertebrate Animal and New In Vitro Models for StudyingPathogens (Basel, Switzerland) · 2023Review
- Immune responses toFrontiers in immunology · 2023Review
- Mechanisms of host manipulation byFrontiers in microbiology · 2023Review
- Variable Expression of Opa Proteins by Neisseria gonorrhoeae Influences Bacterial Association and Phagocytic Killing by Human Neutrophils.Journal of bacteriology · 2022Article
- Acclimation to Nutritional Immunity and Metal Intoxication Requires Zinc, Manganese, and Copper Homeostasis in the PathogenicFrontiers in cellular and infection microbiology · 2022Review
- Neisseria gonorrhoeae subverts formin-dependent actin polymerization to colonize human macrophages.PLoS pathogens · 2021Article
- Transcriptional and Translational Responsiveness of the Neisseria gonorrhoeae Type IV Secretion System to Conditions of Host Infections.Infection and immunity · 2021Article
- Gonococcal Pelvic Inflammatory Disease: Placing Mechanistic Insights Into the Context of Clinical and Epidemiological Observations.The Journal of infectious diseases · 2021Review
- Nonviral sexually transmitted infections in pregnancy: current controversies and new challenges.Current opinion in infectious diseases · 2021Review
- Progesterone SuppressesFrontiers in microbiology · 2021Article
- Influence of Sexually Transmitted Infections in Pregnant Adolescents on Preterm Birth and Chorioamnionitis.Infectious diseases in obstetrics and gynecology · 2020Article
- Intimate Relations: Molecular and Immunologic Interactions BetweenFrontiers in microbiology · 2020Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
An overwhelming neutrophil-driven response causes both acute symptoms and the lasting sequelae that result from infection with Neisseria gonorrhoeae. Neutrophils undergo an aggressive opsonin-independent response to N. gonorrhoeae, driven by the innate decoy receptor CEACAM3. CEACAM3 is exclusively expressed by human neutrophils, and drives a potent binding, phagocytic engulfment and oxidative killing of Opa-expressing bacteria. In this study, we sought to explore the contribution of neutrophils to the pathogenic inflammatory process that typifies gonorrhea. Genome-wide microarray and biochemical profiling of gonococcal-infected neutrophils revealed that CEACAM3 engagement triggers a Syk-, PKCδ- and Tak1-dependent signaling cascade that results in the activation of an NF-κB-dependent transcriptional response, with consequent production of pro-inflammatory cytokines. Using an in vivo model of N. gonorrhoeae infection, we show that human CEACAM-expressing neutrophils have heightened migration toward the site of the infection where they may be further activated upon Opa-dependent binding. Together, this study establishes that the role of CEACAM3 is not restricted to the direct opsonin-independent killing by neutrophils, since it also drives the vigorous inflammatory response that typifies gonorrhea. By carrying the potential to mobilize increasing numbers of neutrophils, CEACAM3 thereby represents the tipping point between protective and pathogenic outcomes of N. gonorrhoeae infection.
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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.