ArticleInfection and immunity2007
Severe tryptophan starvation blocks onset of conventional persistence and reduces reactivation of Chlamydia trachomatis.
Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 89 citations in OpenAlex.
- Non-hematopoietic tryptophan metabolism is a driver of ineffective T cell responses during secondary pulmonary bacterial infection.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Role of IFN-γ from Different Immune Cells inMicroorganisms · 2025Review
- Tryptophan catabolism via the kynurenine pathway regulates infection and inflammation: from mechanisms to biomarkers and therapies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Review
- Advances in vaccine development for Chlamydia trachomatis.Pathogens and disease · 2024Review
- Tryptophan Availability during Persistence of Chlamydia trachomatis Directly Impacts Expression of Chlamydial Cell Division Proteins.Infection and immunity · 2023Article
- Persistence of obligate intracellular pathogens: alternative strategies to overcome host-specific stresses.Frontiers in cellular and infection microbiology · 2023Review
- Association ofFrontiers in cellular and infection microbiology · 2023Article
- Alternative strategies forFrontiers in microbiology · 2022Review
- The role of tryptophan inFrontiers in cellular and infection microbiology · 2022Review
- Article
- Identification of critical amino acid residues in the regulatory N-terminal domain of PMEL.Scientific reports · 2021Article
- Correlation Analysis between Gut Microbiota and Metabolites in Children with Systemic Lupus Erythematosus.Journal of immunology research · 2021Article
- Human Fallopian Tube Epithelial Cell Culture Model To Study Host Responses to Chlamydia trachomatis Infection.Infection and immunity · 2020Article
- Inhibition of tRNA Synthetases Induces Persistence inInfection and immunity · 2020Article
- The Immune Characteristics of the Epididymis and the Immune Pathway of the Epididymitis Caused by Different Pathogens.Frontiers in immunology · 2020Review
- Fecal Metabolites Were Altered, Identified as Biomarkers and Correlated With Disease Activity in Patients With Systemic Lupus Erythematosus in a GC-MS-Based Metabolomics Study.Frontiers in immunology · 2020Article
- Article
- Repeat domain-associated O-glycans govern PMEL fibrillar sheet architecture.Scientific reports · 2019Article
- 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
- Tumor-associated calreticulin variants functionally compromise the peptide loading complex and impair its recruitment of MHC-I.The Journal of biological chemistry · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The intracellular survival of the bacterial pathogen Chlamydia trachomatis depends on protein synthesis by the microbe soon after internalization. Pharmacologic inhibition of bacterial translation inhibits early trafficking of the parasitophorous vacuole (inclusion) to the microtubule-organizing center (MTOC) and promotes its fusion with lysosomes, which is normally blocked by Chlamydia. Depletion of cellular tryptophan pools by gamma interferon-inducible indoleamine-2,3-dioxygenase (IDO) is believed to be the major innate immune mechanism controlling C. trachomatis infection in human cells, an action to which the bacteria can respond by converting into a nonreplicating but highly reactivatable persistent state. However, whether severe IDO-mediated tryptophan starvation can be sufficient to fully arrest the chlamydial life cycle and thereby counteract the onset of persistence is unknown. Here we demonstrate that at low exogenous tryptophan concentrations a substantial fraction of C. trachomatis bacteria fail to traffic to the MTOC or to switch into the conventional persistent state in gamma interferon-induced human cells. The organisms stay scattered in the cell periphery, do not retain infectivity, and display only low transcriptional activity. Importantly, the rate at which these aberrant Chlamydia bacteria become reactivated upon replenishment of cellular tryptophan pools is substantially lower. Thus, severe tryptophan depletion in cells with high IDO activity affects chlamydial development more rigorously than previously described.
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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.