Endometriosis is a debilitating, incurable disease that significantly impacts quality of life, yet the cause remains unknown(1). Emerging research has provided evidence of an association between endometriosis and uterine dysbiosis(2-4). Endogenous antimicrobial peptides and proteins (AMPs) within the female reproductive tract (FTR) act as a first line of defence against pathogens(5). In this study, we aim to assess the presence of three pathogens associated with endometriosis and the dysregulation of AMPs in reproductive biofluids.
Uterine (UF) and peritoneal (PF) fluids were collected using sterile technique from women diagnosed with (n=25) and without endometriosis (n=14). Biofluids were centrifuged to isolate the pellet and supernatant. Genomic DNA was extracted from the pellet, and levels of Fusobacterium nucleatum, Mycoplasma genitalium and Erysipelothrix were quantified and normalised against Eubacteria 16S rRNA, via RT-PCR. The PCR product was visualised using gel electrophoresis. The concentration of AMPs; α-defensin 1, hepcidin and Trappin-2 was quantified using ELISA. Mann-Whitney test was used to determine statistical differences between the groups.
Bacteria were detected in all UF and PF from the control and endo groups, supporting the presence of microbes in the FRT. F. nucleatum was identified in UF in 44% (11/25) of endometriosis patients but was also detected in 21% (3/14) of control participants who had symptoms associated with endometriosis (infertility and dysmenorrhea), although not diagnosed with endometriosis. F. nucleatum was not detected in PF of either group. α-defensin 1 and hepcidin were abundant in the uterine fluid, with increased concentration in the menstrual phase. Although not significant, they were less abundant in the endometriosis group compared to the control group. Trappin-2 also showed a similar pattern among the two groups over different phases of the menstrual cycle.
Our data supports the association of microbes in endometriosis and that uterine dysbiosis may be associated with dysregulation of AMPs.