Dataset Information

Metabolic Reprogramming in Primary Endocervical Cells Infected by Chlamydia trachomatis

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE291078 | GEO | 2025/12/02

REPOSITORIES: GEO

ACCESS DATA

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Project description:Introduction Chlamydia trachomatis (C. trachomatis) is a Gram-negative bacterium and a common human pathogen. The World Health Organization (WHO) estimates that over 130 million people are infected with C. trachomatis globally each year and with increasing incidence. C. trachomatis causes long-lasting and recurrent infections that over time induce severe tissue damage in the female genital tract that can lead to ectopic pregnancy and infertility. Thus, the human immune system fails to control and eradicate C. trachomatis during primary infection and fails to develop protective immunity against secondary infections. In vivo infection models, using complement knock out mice, suggest that the complement system is critically involved in both anti-chlamydial immunity and infection-induced pathology. To increase our understanding of complement-mediated immunity against C. trachomatis we analyzed global complement deposition on serum-incubated C. trachomatis by mass spectrometry. Methods Purified C. trachomatis was incubated in seronegative normal human serum (NHS) or heat-inactivated normal human serum (HI-NHS) for 30 min, thoroughly washed, and processed for mass spectrometry. All samples were lysed, reduced and alkylated and digested with trypsin. Some samples were chemically modified to acetylate free amino groups (N-terminal and lysine amino groups) before trypsin digestion. Peptides were analyzed on a UltimateTM 3500 RSLCnano coupled to a Q Exactive HF-X mass spectrometer. Raw data files were searched against the Uniprot human reference proteome using MaxQuant. Results We demonstrate that C. trachomatis elicits potent complement activation demonstrated by deposition of both early and late complement factors together with several complement regulators. We further demonstrate proteolytically processing of complement C3b to “inactive” C3 cleavage fragments. Conclusion We demonstrate the deposition of several novel complement-associated proteins and -cleavage fragments on the surface of C. trachomatis.

Dataset Information

Metabolic Reprogramming in Primary Endocervical Cells Infected by Chlamydia trachomatis

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets