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Metabolic Reprogramming in Primary Endocervical Cells Infected by Chlamydia trachomatis

GSE291078 Homo sapiens Expression profiling by high throughput sequencing 8 samples Submitted 2025/12/02 Platform GPL24676
Summary
Genital infection by Chlamydia trachomatis is the most common bacterial sexually transmitted disease worldwide, posing a significant threat to reproductive health. Its ability to persist silently in the host often delays treatment, leading to chronic inflammation and complications such as pelvic inflammatory disease, ectopic pregnancy, and infertility in females. Despite progress in understanding C. trachomatis pathogenesis, studies in primary cells remain limited. This study explored the interaction between C. trachomatis and primary human endocervical cells, revealing extensive host transcriptional changes, including strong inflammatory responses (IFN-α, IFN-γ, TNF-α), suppression of E2F targets, DNA repair, G2M checkpoint, and oxidative phosphorylation, indicating mitochondrial dysfunction. Downregulation of electron transport chain genes and phenotypic analysis showed selective TCA cycle impairments in succinate and citrate utilization. Further research is needed to uncover the mechanisms behind C. trachomatis-mitochondria interactions.
Published in
Chlamydia trachomatis disrupts host metabolism in primary cervical epithelial cells
Cheong HC, Rommel MI, Cheok YY et al. · World journal of microbiology & biotechnology 2025 · PMID 41065885 · doi:10.1007/s11274-025-04584-4
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Also filed as BioProject PRJNA1231514 and SRA study SRP567878. Searching any of these in the dataset finder brings you back here.

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