ArticleMicrobial pathogenesis2008
Both leukotoxin and poly-N-acetylglucosamine surface polysaccharide protect Aggregatibacter actinomycetemcomitans cells from macrophage killing.
Article in Microbial pathogenesis, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 47 citations in OpenAlex.
- Biofilms and oral health: nanotechnology for biofilm control.Discover nano · 2025Review
- Review
- Toxin-triggered liposomes for the controlled release of antibiotics to treat infections associated with the gram-negative bacterium, Aggregatibacter actinomycetemcomitans.Colloids and surfaces. B, Biointerfaces · 2024Article
- Modification of Dispersin B with Cyclodextrin-Ciprofloxacin Derivatives for Treating Staphylococcal.Molecules (Basel, Switzerland) · 2023Article
- An in vitro model for studies of attenuation of antibiotic-inhibited growth of Aggregatibacter actinomycetemcomitans Y4 by polyamines.Molecular oral microbiology · 2021Article
- Article
- The Role of Exopolysaccharides in Oral Biofilms.Journal of dental research · 2019Review
- Role of de-N-acetylase PgaB from Aggregatibacter actinomycetemcomitans in exopolysaccharide export in biofilm mode of growth.Molecular oral microbiology · 2017Article
- Aggregatibacter actinomycetemcomitans, a potent immunoregulator of the periodontal host defense system and alveolar bone homeostasis.Molecular oral microbiology · 2016Review
- Structural Basis for Translocation of a Biofilm-supporting Exopolysaccharide across the Bacterial Outer Membrane.The Journal of biological chemistry · 2016Article
- Article
- Azithromycin enhances phagocytic killing of Aggregatibacter actinomycetemcomitans Y4 by human neutrophils.Journal of periodontology · 2015Article
- Role of exopolysaccharide in Aggregatibacter actinomycetemcomitans-induced bone resorption in a rat model for periodontal disease.PloS one · 2015Article
- Article
- The inflammophilic character of the periodontitis-associated microbiota.Molecular oral microbiology · 2014Review
- Sialic acid residues are essential for cell lysis mediated by leukotoxin from Aggregatibacter actinomycetemcomitans.Infection and immunity · 2014Article
- The RNA chaperone Hfq promotes fitness of Actinobacillus pleuropneumoniae during porcine pleuropneumonia.Infection and immunity · 2013Article
- 25-Hydroxyvitamin D(3)-loaded PLA microspheres: in vitro characterization and application in diabetic periodontitis models.AAPS PharmSciTech · 2013Article
- Genome-wide detection of fitness genes in uropathogenic Escherichia coli during systemic infection.PLoS pathogens · 2013Article
- Vesiculation from Pseudomonas aeruginosa under SOS.TheScientificWorldJournal · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Two virulence factors produced by the periodontopathogen Aggregatibacter actinomycetemcomitans are leukotoxin, a secreted lipoprotein that kills human polymorphonuclear leukocytes and macrophages, and poly-N-acetylglucosamine (PGA), a surface polysaccharide that mediates intercellular adhesion, biofilm formation and detergent resistance. In this study we examined the roles of leukotoxin and PGA in protecting A. actinomycetemcomitans cells from killing by the human macrophage cell line THP-1. Monolayers of THP-1 cells were infected with single-cell suspensions of a wild-type A. actinomycetemcomitans strain, or of isogenic leukotoxin or PGA mutant strains. After 48h, viable bacteria were enumerated by dilution plating, macrophage morphology was evaluated microscopically, and macrophage viability was measured by a Trypan blue dye exclusion assay. The number of A. actinomycetemcomitans CFUs increased approximately twofold in wells infected with the wild-type strain, but decreased by approximately 70-90% in wells infected with the leukotoxin and PGA mutant strains. Infection with the wild-type or leukotoxin mutant strain caused a significant decrease in THP-1 cell viability, whereas infection with the PGA mutant strain did not result in any detectable changes in THP-1 viability. Pre-treatment of wild-type A. actinomycetemcomitans cells with the PGA-hydrolyzing enzyme dispersin B rendered them sensitive to killing by THP-1 cells. We concluded that both leukotoxin and PGA are necessary for evasion of macrophage killing by A. actinomycetemcomitans.
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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.