ArticleInfection and immunity2014
Hexa-acylated lipid A is required for host inflammatory response to Neisseria gonorrhoeae in experimental gonorrhea.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 23 citations in OpenAlex.
- Macrophage Proteomic Profiling Reveals Divergent TLR4-Dependent and -Independent Responses to KdoLife (Basel, Switzerland) · 2026Article
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- Resolvin D1 Modulates the Inflammatory Processes of Human Periodontal Ligament Cells via NF-κB and MAPK Signaling Pathways.Biomedicines · 2025Article
- Perturbed CD81 in lung-cancer-derived extracellular vesicles modifies its function in cancer pathophysiology.Molecular therapy. Oncology · 2025Article
- Review
- Progesterone SuppressesFrontiers in microbiology · 2021Article
- Mitochondrial dysfunction caused by outer membrane vesicles from Gram-negative bacteria activates intrinsic apoptosis and inflammation.Nature microbiology · 2020Article
- Outer Membrane Lipid Secretion and the Innate Immune Response to Gram-Negative Bacteria.Infection and immunity · 2020Review
- Bordetella bronchiseptica Glycosyltransferase Core Mutants Trigger Changes in Lipid A Structure.Journal of the American Society for Mass Spectrometry · 2019Article
- Mechanisms of sexually transmitted infection-induced inflammation in women: implications for HIV risk.Journal of the International AIDS Society · 2019Article
- Mechanistic Insight Into the Activation of the NLRP3 Inflammasome byFrontiers in immunology · 2019Article
- Neisseria gonorrhoeae host adaptation and pathogenesis.Nature reviews. Microbiology · 2018Review
- Macrophage-Frontiers in immunology · 2018Review
- Pathogenesis ofFrontiers in immunology · 2018Review
- Article
- Analysis of Bacterial Lipooligosaccharides by MALDI-TOF MS with Traveling Wave Ion Mobility.Journal of the American Society for Mass Spectrometry · 2016Article
- Type I Interferon Induction by Neisseria gonorrhoeae: Dual Requirement of Cyclic GMP-AMP Synthase and Toll-like Receptor 4.Cell reports · 2016Article
- Neisseria gonorrhoeae survives within and modulates apoptosis and inflammatory cytokine production of human macrophages.Cellular microbiology · 2016Article
- Inflammasomes and Their Role in Innate Immunity of Sexually Transmitted Infections.Frontiers in immunology · 2016Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Neisseria gonorrhoeae causes gonorrhea, a sexually transmitted infection characterized by inflammation of the cervix or urethra. However, a significant subset of patients with N. gonorrhoeae remain asymptomatic, without evidence of localized inflammation. Inflammatory responses to N. gonorrhoeae are generated by host innate immune recognition of N. gonorrhoeae by several innate immune signaling pathways, including lipooligosaccharide (LOS) and other pathogen-derived molecules through activation of innate immune signaling systems, including toll-like receptor 4 (TLR4) and the interleukin-1β (IL-1β) processing complex known as the inflammasome. The lipooligosaccharide of N. gonorrhoeae has a hexa-acylated lipid A. N. gonorrhoeae strains that carry an inactivated msbB (also known as lpxL1) gene produce a penta-acylated lipid A and exhibit reduced biofilm formation, survival in epithelial cells, and induction of epithelial cell inflammatory signaling. We now show that msbB-deficient N. gonorrhoeae induces less inflammatory signaling in human monocytic cell lines and murine macrophages than the parent organism. The penta-acylated LOS exhibits reduced toll-like receptor 4 signaling but does not affect N. gonorrhoeae-mediated activation of the inflammasome. We demonstrate that N. gonorrhoeae msbB is dispensable for initiating and maintaining infection in a murine model of gonorrhea. Interestingly, infection with msbB-deficient N. gonorrhoeae is associated with less localized inflammation. Combined, these data suggest that TLR4-mediated recognition of N. gonorrhoeae LOS plays an important role in the pathogenesis of symptomatic gonorrhea infection and that alterations in lipid A biosynthesis may play a role in determining symptomatic and asymptomatic infections.
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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.