Deciphering crucial genes in pelvic inflammatory disease and their relationship with infertility through systems biology studies

Background. Pelvic inflammatory disease (PID) is an infection of the female reproductive system. PID is usually caused by infection with Chlamydia trachomatis (CT) and Neisseria gonorrhoeae (NG). Women with PID have an increased risk of becoming infertility. The aim of this study was to determine the molecular mechanisms that influence infertility and embryonic development in PID with CT and NG infections. Materials and methods. Microarray data were extracted from the Gene Expression Omnibus (GEO), and the protein-protein interaction network was constructed using Cytoscape software. Network analysis was performed to identify hub-bottlenecks and sub-networks. The functional mechanisms for critical genes were identified using the webgestalt server. Results. RPL13, EEF1G, JAK2, MYC, IL7R, CD74, IMPDH2, and NFAT5 were identified as crucial genes in protein-protein interactions and gene regulatory networks in CT and NG infections of PID. Ribosome, hematopoietic cell lineage, platelet activation, and Chagas disease, JAK-STAT pathway, eukaryotic translation elongation, Rap1 pathway, apoptosis, protein processing in the endoplasmic reticulum, progesterone-mediated oocyte maturation, and Epstein–Barr virus infection were identified as significant signaling pathways involving in CT and NG infections. Conclusion. Our model suggests novel critical genes, and functional pathways involved in CT and NG infections, establishing a link between these infections and infertility. However, further studies in vitro and in vivo are needed.