ArticleAntimicrobial agents and chemotherapy2014
The fluoroquinolone levofloxacin triggers the transcriptional activation of iron transport genes that contribute to cell death in Streptococcus pneumoniae.
Article in Antimicrobial agents and chemotherapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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24 citing papers in PubMed, 39 citations in OpenAlex.
- Distribution of DNA gyrase cleavage sites across the Streptococcus pneumoniae genome: relation to transcription and methylation at GATC sites.Nucleic acids research · 2025Article
- Genome-wide antibiotic-CRISPRi profiling identifies LiaR activation as a strategy to resensitize fluoroquinolone-resistant Streptococcus pneumoniae.Nature communications · 2025Article
- Targeted repression ofmBio · 2024Article
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- Machine Learning of Bacterial Transcriptomes Reveals Responses Underlying Differential Antibiotic Susceptibility.mSphere · 2021Article
- Exploring metabolic adaptation of Streptococcus pneumoniae to antibiotics.The Journal of antibiotics · 2020Article
- The TLR4-MyD88 Signaling Axis Regulates Lung Monocyte Differentiation Pathways in Response toFrontiers in immunology · 2020Article
- Reactive Oxygen Species Production Is a Major Factor Directing the Postantibiotic Effect of Fluoroquinolones in Streptococcus pneumoniae.Antimicrobial agents and chemotherapy · 2019Article
- DNA Supercoiling: an Ancestral Regulator of Gene Expression in Pathogenic Bacteria?Computational and structural biotechnology journal · 2019Review
- A Capsular Polysaccharide-Specific Antibody Alters Streptococcus pneumoniae Gene Expression during Nasopharyngeal Colonization of Mice.Infection and immunity · 2018Article
- Tachyplesin Causes Membrane Instability That Kills Multidrug-Resistant Bacteria by Inhibiting the 3-Ketoacyl Carrier Protein Reductase FabG.Frontiers in microbiology · 2018Article
- HU ofFrontiers in microbiology · 2018Article
- Penicillin induces alterations in glutamine metabolism in Streptococcus pneumoniae.Scientific reports · 2017Article
- The Transcriptome ofFrontiers in microbiology · 2017Review
- Treatment of the Fluoroquinolone-Associated Disability: The Pathobiochemical Implications.Oxidative medicine and cellular longevity · 2017Review
- Upregulation of the PatAB Transporter Confers Fluoroquinolone Resistance toFrontiers in microbiology · 2017Article
- Systemic Responses of Multidrug-ResistantFrontiers in cellular and infection microbiology · 2017Article
- Absence of tmRNA Has a Protective Effect against Fluoroquinolones inFrontiers in microbiology · 2016Article
- Reactive Oxygen Species Contribute to the Bactericidal Effects of the Fluoroquinolone Moxifloxacin in Streptococcus pneumoniae.Antimicrobial agents and chemotherapy · 2016Article
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2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
We studied the transcriptomic response of Streptococcus pneumoniae to levofloxacin (LVX) under conditions inhibiting topoisomerase IV but not gyrase. Although a complex transcriptomic response was observed, the most outstanding result was the upregulation of the genes of the fatDCEB operon, involved in iron (Fe(2+) and Fe(3+)) uptake, which were the only genes varying under every condition tested. Although the inhibition of topoisomerase IV by levofloxacin did not have a detectable effect in the level of global supercoiling, increases in general supercoiling and fatD transcription were observed after topoisomerase I inhibition, while the opposite was observed after gyrase inhibition with novobiocin. Since fatDCEB is located in a topological chromosomal domain downregulated by DNA relaxation, we studied the transcription of a copy of the 422-bp (including the Pfat promoter) region located upstream of fatDCEB fused to the cat reporter inserted into the chromosome 106 kb away from its native position: PfatfatD was upregulated in the presence of LVX in its native location, whereas no change was observed in the Pfatcat construction. Results suggest that topological changes are indeed involved in PfatfatDCE transcription. Upregulation of fatDCEB would lead to an increase of intracellular iron and, in turn, to the activation of the Fenton reaction and the increase of reactive oxygen species. In accordance, we observed an attenuation of levofloxacin lethality in iron-deficient media and in a strain lacking the gene coding for SpxB, the main source of hydrogen peroxide. In addition, we observed an increase of reactive oxygen species that contributed to levofloxacin lethality.
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