Abstract
In this study, we investigated the expression profiles of Toll-like receptors(TLRs) in eutopic endometrium(EU) and ectopic endometrium(EC) and its implication in the inflammatory pathogenesis of adenomyosis. Thirty adenomyosis patients who underwent laparoscopy were recruited in this study. We tested the mRNA and protein expression of TLRs, and the mRNA expression of IL-6 and IL-8 in EU and EC of adenomyosis patients, and control endometrium without adenomyosis(CE). We found that the mRNA expression of IL-6 and IL-8 in EU was significantly higher than that in CE, and was the highest in EC (P < 0.01). The mRNA and protein expression of TLRs were higher in EU, with the expression of TLR1-6, 8 and 9 being significantly higher in EU than in CE, and were the highest in EC (except TLR6) (P < 0.05 or P < 0.01). Pearson correlation analysis showed that the expression of TLR1, 2, 4, 5 and 9 in EU and EC was positively correlated with that of IL-6 and IL-8 (P < 0.00139). This study suggested that adenomyosis was a state of inflammatory pathology. High expression of TLRs in EU and EC were positively correlated with IL-6 and IL-8, which may be involved in the inflammatory pathogenesis of adenomyosis.
Highlights
As a special form of endometriosis, adenomyosis is characterized by the presence of heterotopic endometrial glands and stroma within the myometrium[1]
We previously demonstrated that TLR4 was over-expressed in adenomyosis tissues, and the cell model indicated that stromal cells were activated by TLR4 signaling pathway, which processed the cellular inflammatory proliferation and invasive growth involved in the pathogenesis of adenomyosis[14]
Adenomyosis is a benign invasion of the endometrium into the myometrium that is closely related to endometriosis
Summary
As a special form of endometriosis, adenomyosis is characterized by the presence of heterotopic endometrial glands and stroma within the myometrium[1]. Recent evidence indicates that the inflammatory pathogenesis of this disease may be related to the expression of inflammatory mediators, induction of immune response, and genital tract infections as well[7, 8]. Numerous studies have demonstrated that TLR-mediated activation of immune response may be associated with endometriosis and adenomyosis. We previously demonstrated that TLR4 was over-expressed in adenomyosis tissues, and the cell model indicated that stromal cells were activated by TLR4 signaling pathway, which processed the cellular inflammatory proliferation and invasive growth involved in the pathogenesis of adenomyosis[14]. The exact inflammatory pathogenesis of TLR-mediated activation of immune response implicated in the development of adenomyosis remains unclear, and no study to date has reported the expression profiles of TLRs in adenomyosis by measuring all TLRs simultaneously. The aim of the present study was to investigate the expression profiles of TLRs in eutopic endometrium (EU) and ectopic endometrium (EC) to see whether they were truly involved in the inflammatory pathogenesis in adenomyosis
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