ArticleInfection and immunity2013
Peptidoglycan fragment release from Neisseria meningitidis.
Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 51 citations in OpenAlex.
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- Peptidoglycan fragment release and NOD activation by commensalInfection and immunity · 2024Article
- IL-17C is a driver of damaging inflammation during Neisseria gonorrhoeae infection of human Fallopian tube.Nature communications · 2024Article
- Mutation ofJournal of bacteriology · 2023Article
- Bacterial virulence regulation through soluble peptidoglycan fragments sensing and response: knowledge gaps and therapeutic potential.FEMS microbiology reviews · 2023Article
- Success stories of natural product-derived compounds from plants as multidrug resistance modulators in microorganisms.RSC advances · 2023Review
- Mechanisms of host manipulation byFrontiers in microbiology · 2023Review
- The AmiC/NlpD Pathway Dominates Peptidoglycan Breakdown in Neisseria meningitidis and Affects Cell Separation, NOD1 Agonist Production, and Infection.Infection and immunity · 2022Article
- Innate Receptor Activation Patterns Involving TLR and NLR Synergisms in COVID-19, ALI/ARDS and Sepsis Cytokine Storms: A Review and Model Making Novel Predictions and Therapeutic Suggestions.International journal of molecular sciences · 2021Review
- Crosstalk Between Intestinal Serotonergic System and Pattern Recognition Receptors on the Microbiota-Gut-Brain Axis.Frontiers in endocrinology · 2021Review
- Neuronal Damage and Neuroinflammation, a Bridge Between Bacterial Meningitis and Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2021Article
- Synthesis of Bacterial-Derived Peptidoglycan Cross-Linked Fragments.The Journal of organic chemistry · 2020Article
- Neisseria meningitidis: using genomics to understand diversity, evolution and pathogenesis.Nature reviews. Microbiology · 2020Review
- Mini-Review: Bioactivities of Bacterial Cell Envelopes in the Central Nervous System.Frontiers in cellular and infection microbiology · 2020Review
- The Pathogenic Neisseria Use a Streamlined Set of Peptidoglycan Degradation Proteins for Peptidoglycan Remodeling, Recycling, and Toxic Fragment Release.Frontiers in microbiology · 2019Review
- Peptidoglycan Muropeptides: Release, Perception, and Functions as Signaling Molecules.Frontiers in microbiology · 2019Review
- Interplay between Peptidoglycan Biology and Virulence in Gram-Negative Pathogens.Microbiology and molecular biology reviews : MMBR · 2018Review
- Antibiotic Targets in Gonococcal Cell Wall Metabolism.Antibiotics (Basel, Switzerland) · 2018Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Neisseria meningitidis (meningococcus) is a symbiont of the human nasopharynx. On occasion, meningococci disseminate from the nasopharynx to cause invasive disease. Previous work showed that purified meningococcal peptidoglycan (PG) stimulates human Nod1, which leads to activation of NF-κB and production of inflammatory cytokines. No studies have determined if meningococci release PG or activate Nod1 during infection. The closely related pathogen Neisseria gonorrhoeae releases PG fragments during normal growth. These fragments induce inflammatory cytokine production and ciliated cell death in human fallopian tubes. We determined that meningococci also release PG fragments during growth, including fragments known to induce inflammation. We found that N. meningitidis recycles PG fragments via the selective permease AmpG and that meningococcal PG recycling is more efficient than gonococcal PG recycling. Comparison of PG fragment release from N. meningitidis and N. gonorrhoeae showed that meningococci release less of the proinflammatory PG monomers than gonococci and degrade PG to smaller fragments. The decreased release of PG monomers by N. meningitidis relative to N. gonorrhoeae is partly due to ampG, since replacement of gonococcal ampG with the meningococcal allele reduced PG monomer release. Released PG fragments in meningococcal supernatants induced significantly less Nod1-dependent NF-κB activity than released fragments in gonococcal supernatants and tended to induce less interleukin-8 (IL-8) secretion in primary human fallopian tube explants. These results support a model in which efficient PG recycling and extensive degradation of PG fragments lessen inflammatory responses and may be advantageous for maintaining meningococcal carriage in the nasopharynx.
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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.