O-34: Cell Membrane Toll like Receptors Expression in Follicular Cells of Women with Endometriosis

Background: Endometriosis is the growth of endometrial cells outside the uterine cavity. It has been suggested that immune system plays important roles in both initiation and progression of the disease. Several studies have been shown that women with endometriosis diverge in their expression of different genes including heat-shock proteins, fibronectin, and neutrophil elastase, which might be involved in the process of Tolllike receptor (TLR)-dependent sterile inflammation. To date, 10 TLRs are identified in human. TLR1,2,4,5,6 are expressed on the cell membrane. TLRs signaling may lead to change in follicular fluid that is the microenvironment for oocyte development. The aim of this study is to investigate TLRs gene expression in follicular cells obtained from women with endometriosis in comparison to normal women. Materials and Methods: Twenty patients (10 infertile women with endometriosis and 10 normal women with male factor infertility) underwent controlled ovarian stimulation. The follicular fluid was obtained from the largest follicle (>18 mm) then transferred to a sterile Petri dish. After oocytes removal, the fluid was centrifuged at 300g for 5 min. The supernatant was removed. Total RNA was extracted separately from cellular pallet in each group and real time PCR was performed. Results: TLRs genes were expressed in both groups. Although gene expression of TLR1, 2, 5, 6 was higher in endometriosis than normal women but only TLR5 expression was significant. In contrast, TLR4 gene expression was lower in endometriosis than normal women but it wasn’t significant. Conclusion: Our findings suggested that TLRs may be involved in pathophysiology of endometriosis. It was proposed that inflammatory markers such as IL-6, IL-8, IL-12 and TNF-α are elevated in endometriosis. Since these cytokines could be produced by TLRs signaling, therefore it’s possible this alteration is a result of TLRs activation. Our further studies are directed towards understanding TLRs function in endometriosis.