Dysregulated T helper cytokines in serum and peritoneal fluid of women with endometriosis-related infertility
Fadhil Ahsan, Nanda Yuli Rahmawati, M. Y. Ardianta Widyanugraha, Arif Tunjungseto, Sri Ratna Dwiningsih, Ashon Sa'adi, Budi SantosoAbstract
Background
Endometriosis is a chronic inflammatory condition and is one of the leading causes of infertility. The role of T helper (Th) cytokines in infertility remains largely unexamined, despite their recognized importance in endometriosis.
Objectives
To investigate the serum and peritoneal fluid levels of IL-4, IL-5, IL-10, IL-17A, IL-17F, and IFN-γ in women with endometriosis and to explore their correlations with disease severity.
Methods
Eighty-seven infertile women undergoing diagnostic laparoscopy were included, comprising 44 endometriosis patients and 43 controls with benign gynecologic disorders. Serum and peritoneal cytokines were measured using Enzyme-linked immunosorbent assay. Statistical analyses assessed differences and correlations with clinical parameters.
Results
Both serum and peritoneal fluid levels of IL-4 and IL-5 were markedly higher in endometriosis patients compared to controls ( P < 0.001). Although serum IL-10 levels did not show significant differences, there was an increase in peritoneal fluid ( P < 0.001). Among those with endometriosis, serum levels of IL-4, IL-10, IL-17A, and IL-17F exhibited a positive correlation with the revised American Society for Reproductive Medicine score, while IL-17F indicated an inverse correlation with the Endometriosis Fertility Index (EFI) scores ( r = −0.422, P = 0.004). Receiver operating characteristic curve analysis demonstrated that IL-4 and IL-5 effectively distinguished endometriosis cases from controls, with IL-17F also providing significant predictive value for EFI scores ( P = 0.015).
Conclusions
Elevated IL-4 and IL-5 levels in endometriosis suggest a Th2-skewed immune response. Meanwhile, the correlation of IL-17A with disease severity and the inverse relationship of IL-17F with fertility scores highlight the complex role of the Th17 response. These findings enhance understanding of cytokine dysregulation in endometriosis and may guide future therapeutic strategies.