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c-Myc plays a key role in IFN-γ-induced persistence of Chlamydia trachomatis

by Guo, Yongxia , Kurmasheva, Naziia , Schlicker, Lisa , Janaki-Raman, Sudha , Rudel, Thomas , Hovhannisyan, Pargev , Schmitz, Werner , Stelzner, Kathrin , Rajeeve, Karthika , Vollmuth, Nadine , Schulze, Almut

in 1-Phosphatidylinositol 3-kinase / Biosynthesis / c-Myc / c-Myc protein / Cell division / Cell growth / Cell lines / Chlamydia / Chlamydia trachomatis / Cytokines / Dioxygenase / Fallopian tube / Genomes / Immune system / Infections / interferon-gamma / Intermediates / Kinases / Metabolism / Microbiology and Infectious Disease / Myc protein / Organoids / Pathogens / persistence / Phosphorylation / Sexually transmitted diseases / Stat1 protein / STD / Tricarboxylic acid cycle / Tryptophan / γ-Interferon

2022

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c-Myc plays a key role in IFN-γ-induced persistence of Chlamydia trachomatis

2022

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c-Myc plays a key role in IFN-γ-induced persistence of Chlamydia trachomatis

2022

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Journal Article

c-Myc plays a key role in IFN-γ-induced persistence of Chlamydia trachomatis

Guo, Yongxia,

Kurmasheva, Naziia,

Schlicker, Lisa,

Janaki-Raman, Sudha,

Rudel, Thomas,

Hovhannisyan, Pargev,

Schmitz, Werner,

Stelzner, Kathrin,

Rajeeve, Karthika,

Vollmuth, Nadine,

Schulze, Almut

2022

Overview

Chlamydia trachomatis (Ctr) can persist over extended times within their host cell and thereby establish chronic infections. One of the major inducers of chlamydial persistence is interferon-gamma (IFN-γ) released by immune cells as a mechanism of immune defence. IFN-γ activates the catabolic depletion of L-tryptophan (Trp) via indoleamine-2,3-dioxygenase (IDO), resulting in persistent Ctr . Here, we show that IFN-γ induces the downregulation of c-Myc, the key regulator of host cell metabolism, in a STAT1-dependent manner. Expression of c-Myc rescued Ctr from IFN-γ-induced persistence in cell lines and human fallopian tube organoids. Trp concentrations control c-Myc levels most likely via the PI3K-GSK3β axis. Unbiased metabolic analysis revealed that Ctr infection reprograms the host cell tricarboxylic acid (TCA) cycle to support pyrimidine biosynthesis. Addition of TCA cycle intermediates or pyrimidine/purine nucleosides to infected cells rescued Ctr from IFN-γ-induced persistence. Thus, our results challenge the longstanding hypothesis of Trp depletion through IDO as the major mechanism of IFN-γ-induced metabolic immune defence and significantly extends the understanding of the role of IFN-γ as a broad modulator of host cell metabolism.

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Publisher

eLife Sciences Publications Ltd,eLife Sciences Publications, Ltd

Subject

1-Phosphatidylinositol 3-kinase

/ c-Myc