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Sex hormones alter the response of Toll-like receptor 3 to its specific ligand in fallopian tube epithelial cells

  • Zandieh, Zahra (Shahid Akbar Abadi Clinical Research Development Unit, Iran University of Medical Sciences) ;
  • Amjadi, Fatemehsadat (Department of Anatomy, School of Medicine, Iran University of Medical Sciences) ;
  • Vakilian, Haghighat (Department of Nanobiotechnology, Faculty of Biological Sciences, Tarbiat Modares University) ;
  • Aflatoonian, Khashayar (School of Medicine, Iran University of Medical Sciences) ;
  • Amirchaghmaghi, Elham (Department of Regenerative Biomedicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR) ;
  • Fazeli, Alireza (Academic Unit of Reproductive and Developmental Medicine, The University of Sheffield) ;
  • Aflatoonian, Reza (Department of Endocrinology and Female Infertility, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR)
  • Received : 2018.02.20
  • Accepted : 2018.10.16
  • Published : 2018.12.31

Abstract

Objective: The fallopian tubes play a critical role in the early events of fertilization. The rapid innate immune defense is an important part of the fallopian tubes. Toll-like receptor 3 (TLR3), as a part of the innate immune system, plays an important role in detecting viral infections. In this basic and experimental study, the effect of sex hormones on the function of TLR3 in the OE-E6/E7 cell line was investigated. Methods: The functionality of TLR3 in this cell line was evaluated by cytokine measurements (interleukin [IL]-6 and IL-1b) and the effects of sex hormones on TLR3 were tested by an enzyme-linked immunosorbent assay kit. Additionally, TLR3 small interfering RNA (siRNA) and a TLR3 function-blocking antibody were used to confirm our findings. Results: The production of IL-6 significantly increased in the presence of polyinosinic-polycytidylic acid (poly(I:C)) as the TLR3 ligand. Using a TLR3-siRNA-ransfected OE-E6/E7 cell line and function-blocking antibody confirmed that cytokine production was due to TLR3. In addition, 17-${\beta}$ estradiol and progesterone suppressed the production of IL-6 in the presence and absence of poly(I:C). Conclusion: These results imply that sex hormones exerted a suppressive effect on the function of TLR3 in the fallopian tube cell line when different concentrations of sex hormones were present. The current results also suggest that estrogen receptor beta and nuclear progesterone receptor B are likely to mediate the hormonal regulation of TLR3, as these two receptors are the main estrogen and progesterone receptors in OEE6/E7 cell line.

Keywords

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