Chlamydia trachomatis disrupts host metabolism in primary cervical epithelial cells.

Abstract

Chlamydia trachomatis is a major cause of bacterial sexually transmitted infections and reproductive complications. Despite progress in understanding C. trachomatis pathogenesis, studies using primary cells remain limited. Here, we investigated C. trachomatis infection of cervical epithelial cells and its impact on host cellular processes. Transcriptomic profiling show that C. trachomatis infection in cervical epithelial cells leads to significant changes in host cellular processes, including modulation of immune signaling, attenuation of DNA repair and proliferation-linked signaling pathways, as well as disruption of mitochondrial function. Mitochondrial substrate utilization assays revealed selective TCA cycle impairments. Our findings show that C. trachomatis infection is associated with marked changes of host cell metabolism and mitochondrial function. These findings suggest that metabolic rewiring in cervical epithelial cells may reflect a host defense strategy to restrict pathogen. Our results provide novel insights into the metabolic interplay between host and C. trachomatis and open avenues for future investigations into the consequences of metabolic remodeling during chlamydial infection.