ArticleInfection and immunity2011
Inhibition of indoleamine 2,3-dioxygenase activity by levo-1-methyl tryptophan blocks gamma interferon-induced Chlamydia trachomatis persistence in human epithelial cells.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 58 citations in OpenAlex.
- Mechanisms, management and prevention of anorectal sexually transmitted infections.Nature reviews. Gastroenterology & hepatology · 2026Review
- Integrated multi-omics analysis uncovers cervicovaginal ecological networks and their association withInfection and immunity · 2026Article
- Goblet of fire: how Chlamydia ignites region-specific colitis by hijacking goblet cells.The Journal of clinical investigation · 2026Article
- Pathobiont-triggered induction of goblet cell response drives regional susceptibility to inflammatory bowel disease.The Journal of clinical investigation · 2026Article
- Cytotoxic CD4+ T Cells Are Induced during Infection with Chlamydia trachomatis.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Host Cell Amplification of Nutritional Stress Contributes To Persistence in Chlamydia trachomatis.mBio · 2022Article
- The role of tryptophan inFrontiers in cellular and infection microbiology · 2022Review
- Article
- Resistance of Mycobacterium tuberculosis to indole 4-carboxamides occurs through alterations in drug metabolism and tryptophan biosynthesis.Cell chemical biology · 2021Article
- Genome copy number regulates inclusion expansion, septation, and infectious developmental form conversion inJournal of bacteriology · 2021Article
- [Postinfectious reactive arthritis after chlamydia infection in competitive sports : Clinical management and current literature review].Der Orthopade · 2021Review
- IL-10Frontiers in immunology · 2021Article
- Article
- Indoleamine 2,3-Dioxygenase Cannot InhibitFrontiers in immunology · 2021Article
- The iron-dependent repressor YtgR is a tryptophan-dependent attenuator of the trpRBA operon in Chlamydia trachomatis.Nature communications · 2020Article
- Inhibition of tRNA Synthetases Induces Persistence inInfection and immunity · 2020Article
- Host cell depletion of tryptophan by IFNγ-induced Indoleamine 2,3-dioxygenase 1 (IDO1) inhibits lysosomal replication of Coxiella burnetii.PLoS pathogens · 2019Article
- Tryptophan metabolism as a common therapeutic target in cancer, neurodegeneration and beyond.Nature reviews. Drug discovery · 2019Review
- Indoleamine 2, 3-Dioxygenase-Mediated Tryptophan Catabolism: A Leading Star or Supporting Act in the Tuberculosis and HIV Pas-de-Deux?Frontiers in cellular and infection microbiology · 2019Review
- Chlamydia trachomatis-infected cells and uninfected-bystander cells exhibit diametrically opposed responses to interferon gamma.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
Gamma interferon (IFN-γ) induces expression of the tryptophan-catabolizing enzyme indoleamine 2,3-dioxygenase (IDO1) in human epithelial cells, the permissive cells for the obligate intracellular bacterium Chlamydia trachomatis. IDO1 depletes tryptophan by catabolizing it to kynurenine with consequences for C. trachomatis, which is a tryptophan auxotroph. In vitro studies reveal that tryptophan depletion can result in the formation of persistent (viable but noncultivable) chlamydial forms. Here, we tested the effects of the IDO1 inhibitor, levo-1-methyl-tryptophan (L-1MT), on IFN-γ-induced C. trachomatis persistence. We found that addition of 0.2 mM L-1MT to IFN-γ-exposed infected HeLa cell cultures restricted IDO1 activity at the mid-stage (20 h postinfection [hpi]) of the chlamydial developmental cycle. This delayed tryptophan depletion until the late stage (38 hpi) of the cycle. Parallel morphological and gene expression studies indicated a consequence of the delay was a block in the induction of C. trachomatis persistence by IFN-γ. Furthermore, L-1MT addition allowed C. trachomatis to undergo secondary differentiation, albeit with limited productive multiplication of the bacterium. IFN-γ-induced persistent infections in epithelial cells have been previously reported to be more resistant to doxycycline than normal productive infections in vitro. Pertinent to this observation, we found that L-1MT significantly improved the efficacy of doxycycline in clearing persistent C. trachomatis forms. It has been postulated that persistent forms of C. trachomatis may contribute to chronic chlamydial disease. Our findings suggest that IDO1 inhibitors such as L-1MT might provide a novel means to investigate, and potentially target, persistent chlamydial forms, particularly in conjunction with conventional therapeutics.
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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.