ArticlemBio2014
A 2-pyridone-amide inhibitor targets the glucose metabolism pathway of Chlamydia trachomatis.
Article in mBio, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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
11 citing papers in PubMed.
- Metabolism and physiology of pathogenic bacterial obligate intracellular parasites.Frontiers in cellular and infection microbiology · 2024Review
- A 2-pyridone amide inhibitor of transcriptional activity inAntimicrobial agents and chemotherapy · 2023Article
- Differential Effects of Small Molecule Inhibitors on the Intracellular Chlamydia Infection.mBio · 2022Article
- The Small Molecule H89 InhibitsInfection and immunity · 2021Article
- Genome copy number regulates inclusion expansion, septation, and infectious developmental form conversion inJournal of bacteriology · 2021Article
- Methyl sulfonamide substituents improve the pharmacokinetic properties of bicyclic 2-pyridone basedMedChemComm · 2019Article
- Red FluorescentFrontiers in microbiology · 2018Article
- Chlamydia trachomatis Prevents Apoptosis Via Activation of PDPK1-MYC and Enhanced Mitochondrial Binding of Hexokinase II.EBioMedicine · 2017Article
- Growth ofFrontiers in cellular and infection microbiology · 2017Article
- Active Transport of Phosphorylated Carbohydrates Promotes Intestinal Colonization and Transmission of a Bacterial Pathogen.PLoS pathogens · 2015Article
- Chlamydia trachomatis In Vivo to In Vitro Transition Reveals Mechanisms of Phase Variation and Down-Regulation of Virulence Factors.PloS one · 2015Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
unlabelledIn a screen for compounds that inhibit infectivity of the obligate intracellular pathogen Chlamydia trachomatis, we identified the 2-pyridone amide KSK120. A fluorescent KSK120 analogue was synthesized and observed to be associated with the C. trachomatis surface, suggesting that its target is bacterial. We isolated KSK120-resistant strains and determined that several resistance mutations are in genes that affect the uptake and use of glucose-6-phosphate (G-6P). Consistent with an effect on G-6P metabolism, treatment with KSK120 blocked glycogen accumulation. Interestingly, KSK120 did not affect Escherichia coli or the host cell. Thus, 2-pyridone amides may represent a class of drugs that can specifically inhibit C. trachomatis infection. IMPORTANCE: Chlamydia trachomatis is a bacterial pathogen of humans that causes a common sexually transmitted disease as well as eye infections. It grows only inside cells of its host organism, within a parasitophorous vacuole termed the inclusion. Little is known, however, about what bacterial components and processes are important for C. trachomatis cellular infectivity. Here, by using a visual screen for compounds that affect bacterial distribution within the chlamydial inclusion, we identified the inhibitor KSK120. As hypothesized, the altered bacterial distribution induced by KSK120 correlated with a block in C. trachomatis infectivity. Our data suggest that the compound targets the glucose-6-phosphate (G-6P) metabolism pathway of C. trachomatis, supporting previous indications that G-6P metabolism is critical for C. trachomatis infectivity. Thus, KSK120 may be a useful tool to study chlamydial glucose metabolism and has the potential to be used in the treatment of C. trachomatis infections.
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Registered trials
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