P-82: The Role of Toll-Like Receptor 2 in Ectopic Pregnancy
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Abstract:
Background: The innate immune system is our first line of defense against invading pathogens. Toll–like receptors (TLRs) have been identified as a key role in mediating the function of innate immune system which bridges the gap between innate and adaptive immunity. For example, TLR2 is able to act as a homodimer to recognize lipoteichoic acids of Gram-positive bacteria but as a heterodimer with TLR1 or TLR6 to recognize triacylated lipoproteins and diacylated lipoproteins, respectively. Functional roles of TLR in the female reproductive tract health are important and will elucidate the complexity of immunological events impacting on pregnancy. Ectopic Pregnancy (EP) is a pregnancy where the fertilized egg implants outside the uterus and it often occurs in the Fallopian Tube (FT). Thus, the objective of this study is investigation TLR2 expression in FTs carrying EP. Materials and Methods: Biopsies from Infundibulum, Ampulla and Isthmus of FT were obtained from women who underwent hysterectomy and salpingectomy for EP. Human chorionic gonadotropin (HCG) was injected in 14 days leading up to hysterectomy to produce a state of pseudo-pregnancy. In this study pseudo-pregnants are control group and ectopic pregnants are case group. RT-PCR was used to test the existence of TLR2 gene in these sections. FT from pseudo-pregnants and ectopic pregnants were compared with Q-PCR for TLR2 gene. Results: By using RT-PCR, TLR2 expression has found in Infundibulum, Ampulla and Isthmus from case and control group. Q-PCR has shown relative TLR2 expression in all parts of FT from control group is stronger than case group. Conclusion: Besides TLRs role in protection against invading microorganisms in the female reproductive tract, growing evidence suggests an important role for TLRs in mediating several interactions occurring between the immune and reproductive system. It is likely that turning down of TLR2 expression in FT can predispose to ectopic pregnancy.
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volume 5 issue Supplement Issue
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publication date 2011-09-01
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