ArticleScientific reports2016
The biofilm inhibitor Carolacton inhibits planktonic growth of virulent pneumococci via a conserved target.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 25 citations in OpenAlex.
- In Situ Biofilm Affinity-Based Protein Profiling Identifies the Streptococcal Hydrolase GbpB as the Target of a Carolacton-Inspired Chemical Probe.Journal of the American Chemical Society · 2024Article
- An Update on Pharmacological Relevance and Chemical Synthesis of Natural Products and Derivatives with Anti SARS-CoV-2 Activity.ChemistrySelect · 2021Review
- Insights into 6S RNA in lactic acid bacteria (LAB).BMC genomic data · 2021Article
- Natural Products and Derivatives Targeting at Cancer Energy Metabolism: A Potential Treatment Strategy.Current medical science · 2020Review
- Deep sequencing of biofilm microbiomes on dental composite materials.Journal of oral microbiology · 2019Article
- Honokiol-Inspired Analogs as Inhibitors of Oral Bacteria.ACS infectious diseases · 2018Article
- The natural product carolacton inhibits folate-dependent C1 metabolism by targeting FolD/MTHFD.Nature communications · 2017Article
- Natural Products as Platforms To Overcome Antibiotic Resistance.Chemical reviews · 2017Review
- Complete Genome Sequences of Three Multidrug-Resistant Clinical Isolates ofGenome announcements · 2017Article
- Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
New antibacterial compounds, preferentially exploiting novel cellular targets, are urgently needed to fight the increasing resistance of pathogens against conventional antibiotics. Here we demonstrate that Carolacton, a myxobacterial secondary metabolite previously shown to damage Streptococcus mutans biofilms, inhibits planktonic growth of Streptococcus pneumoniae TIGR4 and multidrug-resistant clinical isolates of serotype 19A at nanomolar concentrations. A Carolacton diastereomer is inactive in both streptococci, indicating a highly specific interaction with a conserved cellular target. S. mutans requires the eukaryotic-like serine/threonine protein kinase PknB and the cysteine metabolism regulator CysR for susceptibility to Carolacton, whereas their homologues are not needed in S. pneumoniae, suggesting a specific function for S. mutans biofilms only. A bactericidal effect of Carolacton was observed for S. pneumoniae TIGR4, with a reduction of cell numbers by 3 log units. The clinical pneumonia isolate Sp49 showed immediate growth arrest and cell lysis, suggesting a bacteriolytic effect of Carolacton. Carolacton treatment caused a reduction in membrane potential, but not membrane integrity, and transcriptome analysis revealed compensatory reactions of the cell. Our data show that Carolacton might have potential for treating pneumococcal infections.
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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.