ArticlePloS one2011
NafA negatively controls Neisseria meningitidis piliation.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 13 citations in OpenAlex.
- Pilus-mediated co-aggregation with Lactobacillus crispatus increases meningococcal susceptibility to antimicrobial agents by interfering with microcolony formation.BMC microbiology · 2025Article
- Vertebrate and Invertebrate Animal and New In Vitro Models for StudyingPathogens (Basel, Switzerland) · 2023Review
- Lactate-Induced Dispersal ofInfection and immunity · 2021Article
- Deletion of D-Lactate Dehydrogenase A inFrontiers in microbiology · 2019Article
- The primary transcriptome of Neisseria meningitidis and its interaction with the RNA chaperone Hfq.Nucleic acids research · 2017Article
- Host cell-derived lactate functions as an effector molecule in Neisseria meningitidis microcolony dispersal.PLoS pathogens · 2017Article
- Neisseria meningitidis Polynucleotide Phosphorylase Affects Aggregation, Adhesion, and Virulence.Infection and immunity · 2016Article
- Characterization of a novel antisense RNA in the major pilin locus of Neisseria meningitidis influencing antigenic variation.Journal of bacteriology · 2015Article
- Characterization of motility and piliation in pathogenic Neisseria.BMC microbiology · 2015Article
- Transcriptional profiling of Neisseria meningitidis interacting with human epithelial cells in a long-term in vitro colonization model.Infection and immunity · 2013Article
- Type IV pilin proteins: versatile molecular modules.Microbiology and molecular biology reviews : MMBR · 2012Review
- Loss of meningococcal PilU delays microcolony formation and attenuates virulence in vivo.Infection and immunity · 2012Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bacterial auto-aggregation is a critical step during adhesion of N. meningitidis to host cells. The precise mechanisms and functions of bacterial auto-aggregation still remain to be fully elucidated. In this work, we characterize the role of a meningococcal hypothetical protein, NMB0995/NMC0982, and show that this protein, here denoted NafA, acts as an anti-aggregation factor. NafA was confirmed to be surface exposed and was found to be induced at a late stage of bacterial adherence to epithelial cells. A NafA deficient mutant was hyperpiliated and formed bundles of pili. Further, the mutant displayed increased adherence to epithelial cells when compared to the wild-type strain. In the absence of host cells, the NafA deficient mutant was more aggregative than the wild-type strain. The in vivo role of NafA in sepsis was studied in a murine model of meningococcal disease. Challenge with the NafA deficient mutant resulted in lower bacteremia levels and mortality when compared to the wild-type strain. The present study reveals that meningococcal NafA is an anti-aggregation factor with strong impact on the disease outcome. These data also suggest that appropriate bacterial auto-aggregation is controlled by both aggregation and anti-aggregation factors during Neisseria infection in vivo.
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Registered trials
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