ArticleCellular microbiology2019
Evaluating the role of Burkholderia pseudomallei K96243 toxins BPSS0390, BPSS0395, and BPSS1584 in persistent infection.
Article in Cellular microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 23 citations in OpenAlex.
- Discovery of repurposed drugs that disrupt intracellular replication of Burkholderia pseudomallei and Burkholderia mallei and protect against lethal aerosol infection.PLoS pathogens · 2026Article
- Trigger Factor inJournal of bacteriology · 2026Article
- The Characterization of a Gonococcal HicAB Toxin-Antitoxin System Capable of Causing Bacteriostatic Growth Arrest.Microorganisms · 2025Article
- The HicAB System: Characteristics and Biological Roles of an Underappreciated Toxin-Antitoxin System.International journal of molecular sciences · 2024Review
- The plasmid-borne hipBA operon of Klebsiella michiganensis encodes a potent plasmid stabilization system.Journal of applied microbiology · 2024Article
- Host stress drives tolerance and persistence: The bane of anti-microbial therapeutics.Cell host & microbe · 2024Review
- Intracellular persister: A stealth agent recalcitrant to antibiotics.Frontiers in cellular and infection microbiology · 2023Review
- Evaluating the Contribution of the Predicted Toxin-Antitoxin System HigBA to Persistence, Biofilm Formation, and Virulence in Burkholderia pseudomallei.Infection and immunity · 2022Article
- Characterization of the Key Determinants of Phd Antitoxin Mediated Doc Toxin Inactivation inACS chemical biology · 2022Article
- GNAT toxins evolve toward narrow tRNA target specificities.Nucleic acids research · 2022Article
- Auxiliary interfaces support the evolution of specific toxin-antitoxin pairing.Nature chemical biology · 2021Article
- Methods for Enrichment of Bacterial Persister Populations for Phenotypic Screens and Genomic Studies.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Review
- Multinucleated Giant Cell Formation as a Portal to Chronic Bacterial Infections.Microorganisms · 2020Review
- Predicting toxins found in toxin-antitoxin systems with a role in host-induced Burkholderia pseudomallei persistence.Scientific reports · 2020Article
- What Can Go Wrong When Applying Immune Modulation Therapies to Target Persistent Bacterial Infections.Journal of cellular immunology · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Burkholderia pseudomallei is the causative agent of melioidosis, a disease with a mortality rate of up to 40% even with treatment. Despite the ability of certain antibiotics to control initial infection, relapse occurs in treated patients. The inability of antibiotics to clear this bacterial infection is in part due to persistence, an evasion mechanism against antibiotics and the effect of host defenses. Evaluation of antibiotic efficacy against B. pseudomallei revealed that up to 48% of in vitro grown populations can survive in a persister state. Toxin-antitoxin (TA) systems have been previously implicated in modulating bacterial persistence. We generated three isogenic TA mutants and found that loss of each toxin gene did not alter antibiotic persistence or macrophage survival. In response to macrophage-induced persistence, all three toxin mutants demonstrated increased intracellular susceptibility to levofloxacin which in part was due to the inability of the mutants to induce persistence after nitric oxide or nutrient starvation. In an inhalational model of murine melioidosis, both ΔBPSS0395 and ΔBPSS1584 strains were attenuated, and treatment with levofloxacin led to significant reduction in lung colonisation and reduced splenic colonisation by ΔBPSS0395. Based on our findings, these toxins deserve additional evaluation as putative therapeutic targets.
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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.