Metabolic Reprogramming in Primary Endocervical Cells Infected by Chlamydia trachomatis

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-a, IFN-?, TNF-a), 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. Overall design: RNA-seq profiling of primary endocervical cells (PCS-480-011) infected by C. trachomatis for 8, 24, and 40 hours.