Author/Authors :
Zandieh، Zahra نويسنده Department of Anatomy, School of Medicine Sciences, Iran University of Medical Sciences, Tehran, Iran. Zandieh, Zahra , Amjadi، Fatemehsadat نويسنده Department of Anatomy, Tehran University of Medical Sciences, Tehran, Iran. , , Ashrafi، Mahnaz نويسنده , , Aflatoonian، Abbas نويسنده , , Fazeli، Alireza نويسنده , , Aflatoonian، Mohammad Reza نويسنده ,
Abstract :
Objective: Toll like receptors (TLRs) are one of the main components of the innate immune
system. It has been reported that expression of these receptors are altered in the
female reproductive tract (FRT) during menstrual cycle. Here we used a fallopian tube
epithelial cell line (OE-E6/E7) to evaluate the effect of two sex hormones in modulating
TLR expression.
Materials and Methods: In this experimental study, initially TLR gene expression in OEE6/
E7 cells was evaluated and compared with that of fallopian tube tissue using quantitative
real time-polymerase chain reaction (qRT-PCR) and immunostaining. Thereafter,
OE-E6/E7 cells were cultured with different concentrations of estradiol and progesterone,
and combination of both. qRT-PCR was performed to reveal any changes in expression of
TLR genes as a result of hormonal treatment.
Results: TLR1-10 genes were expressed in human fallopian tube tissue. TLR1-6 genes
and their respective proteins were expressed in the OE-E6/E7 cell line. Although estradiol
and progesterone separately had no significant effect on TLR expression, their combined
treatment altered the expression of TLRs in this cell line. Also, the pattern of TLR expression
in preovulation (P), mensturation (M) and window of implantation (W) were the same
for all TLRs with no significant differences between P, M and W groups.
Conclusion: These data show the significant involvement of the combination of estradiol
and progesterone in modulation of TLR gene expression in this human fallopian
tube cell line. Further experiments may reveal the regulatory mechanism and
signalling pathway behind the effect of sex hormones in modulating TLRs in the human
FRT.