ArticleScientific reports2018
Chlamydia trachomatis-infected cells and uninfected-bystander cells exhibit diametrically opposed responses to interferon gamma.
Article in Scientific reports, 2018. 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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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- Chlamydia trachomatis disrupts host metabolism in primary cervical epithelial cells.World journal of microbiology & biotechnology · 2025Article
- ThebioRxiv : the preprint server for biology · 2025Article
- Could the COVID-19-Driven Increased Use of Ivermectin Lead to Incidents of Imbalanced Gut Microbiota and Dysbiosis?Probiotics and antimicrobial proteins · 2022Review
- The role of tryptophan inFrontiers in cellular and infection microbiology · 2022Review
- Reprogramming of microRNA expression via E2F1 downregulation promotes Salmonella infection both in infected and bystander cells.Nature communications · 2021Article
- Circulating immunity protects the female reproductive tract fromProceedings of the National Academy of Sciences of the United States of America · 2021Article
- To Kill But Not Be Killed: Controlling the Activity of Mammalian Pore-Forming Proteins.Frontiers in immunology · 2020Review
- Ammonia generation by tryptophan synthase drives a key genetic difference between genital and ocularProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Alternatively Activated Macrophages Are Host Cells forFrontiers in microbiology · 2019Article
- Genetic Transformation of aFrontiers in cellular and infection microbiology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
The intracellular bacterial pathogen, Chlamydia trachomatis, is a tryptophan auxotroph. Therefore, induction of the host tryptophan catabolizing enzyme, indoleamine-2,3-dioxgenase-1 (IDO1), by interferon gamma (IFNγ) is one of the primary protective responses against chlamydial infection. However, despite the presence of a robust IFNγ response, active and replicating C. trachomatis can be detected in cervical secretions of women. We hypothesized that a primary C. trachomatis infection may evade the IFNγ response, and that the protective effect of this cytokine results from its activation of tryptophan catabolism in bystander cells. To test this hypothesis, we developed a novel method to separate a pool of cells exposed to C. trachomatis into pure populations of live infected and bystander cells and applied this technique to distinguish between the effects of IFNγ on infected and bystander cells. Our findings revealed that the protective induction of IDO1 is suppressed specifically within primary infected cells because Chlamydia attenuates the nuclear import of activated STAT1 following IFNγ exposure, without affecting STAT1 levels or phosphorylation. Critically, the IFNγ-mediated induction of IDO1 activity is unhindered in bystander cells. Therefore, the IDO1-mediated tryptophan catabolism is functional in these cells, transforming these bystander cells into inhospitable hosts for a secondary C. trachomatis infection.
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