P-189: Gene Variations of Toll-Like Receptor 2 in Endometriosis

Background: Endometriosis, a common, benign, estrogendependent and chronic inflammatory condition, is characterized by the ectopic growth of endometrial tissue that is found primarily in the peritoneum, ovaries and rectovaginal septum. In addition to its usual description as a hormonal disorder, some genetic, immunological and environmental factors can affect this disease. Toll-like receptors (TLRs) constitute a family of pattern recognition receptors, recognizing a variety of exogenous and endogenous ligands playing the key role in innate immune response. Also they would be involved in cell proliferation processes, apoptosis, angiogenesis, tissue remodeling and repair. Since TLR2 expression decline has been observed in endometriosis in our group, we decided to study the genetic variations of TLR2, as well. Materials and Methods: In this case-control study, 70 DNA samples were recruited from endometriosis patients who had been confirmed by laparoscopic surgery and 55 fertile women as control group that no history of inflammatory disorders or using any related drugs. All DNA samples were obtained from Royan DNA bank that had been extracted from peripheral blood along 2012-14. The LRR regions of TLR2 in exon3 divided into 2 fragments were amplified by polymerase chain reaction (PCR) and products were analyzed by sequencing. Results: In the first fragment, Synonymous Single Nucleotide Polymorphism (SNP) (rs3804099) C/T was observed in 48 out of 70 patients (68.5%), and 29 out of 55 controls (52.7%), while 12 patients (17.1%) and 9 controls (16.3%), had shown Synonymous SNP (rs3804100) C/T in the second fragment. Observed SNPs’ locations are in LRR6 and LRR11, respectively. The present study showed that the SNP frequencies between patients and controls, were not significantly different (p=0.07). Conclusion: Although both of these SNPs are very common in inflammatory disorders, only SNP (rs3804099) was observed more in both groups of our studied population.