Abstract
their surface, but they expressed TLR4 intracellularly as judged bywestern blotting. BothWECs and ESCs expressed TLR4 and MyD88 transcripts. In contrary to ESCs, whole endometrial cells also expressed substantial amounts of TLR2. LPS stimulation increased TLR4 gene expression in both cell types, but this was not statistically significant, whereas treatment with LPS after 8hours significantly increased MyD88 gene expression. Also, LTA increased TLR2 andMyD88 gene expression, but thiswas not reached to statistically significant level. LPS and LTA increased production of TNF, IL-6 and IL-8 in ESCs and WECs in a dose-dependent manner. VD3 significantly decreased expression of MyD88 gene in ESCs in both LPS-treated and control cells, but did not have significant effect on TLR-2 and 4 expressions. Vitamin D3 treatment resulted in substantial decrease of TNFand IL-6 production by LPSand LTAstimulated cells, whereas increased IL-8 production. CONCLUSIONS: These findings imply that TLRs are among the first defensemechanism of innate immune system at the female reproductive tract. In the same time, triggering TLRs during pregnancy by ascending bacterial infections may mediate inflammatory cytokine release which could potentially be harmful to developing fetus. Based on the results presented here, it seems that vitamin D3 could control adverse effects associated with female reproductive tract infection throughmodulation ofMyD88 expression, an adaptor protein which play essential role in TLR signaling cascade. Based on these findings, we propose vitamin D3 as a novel natural therapeutic compound for threatened pregnancies due to genital tract infections.
Published Version
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