Abstract
Summary Sentence The role of microbial and immunological menstrual cycle dependent changes within the endometrium may provide insight into the underlying causes of dysfunctional menstrual cycles. Abstract The ovarian steroid hormones control cyclic cellular proliferation, differentiation, inflammatory cell recruitment, apoptosis, tissue degradation and regeneration associated with the menstrual cycle as well as the response to pathogen challenge. Women with dysfunctional menstrual cycles (menorrhagia and dysmenorrhea) exhibit altered cytokine and prostaglandin expression in the endometrium implying ongoing recruitment of innate immune mediators. Activation of TLRs by endogenous and/or exogenous ligands caused by cell damage resulting from ongoing inflammation, endogenous microbiota or dysbiosis may contribute to the inflammatory symptoms associated with these conditions. The role of the upper genital tract endogenous microbiota in promoting genital tract homeostasis through possible promotion of re-epithelialization or anti-inflammatory mediators warrants further investigation.
Highlights
Constant activation of Toll-like receptors (TLR) during prolonged bleeding, inflammation and repair may reduce the threshold for TLR activation by exogenous ligands leading to hyper-responsiveness to pathogen associated molecular patterns (PAMPs) recognition leading to ongoing inflammation and pathology
Subacute inflammation associated with dysbiosis in the endogenous endometrial microbiota in women with primary menorrhagia and/ or dysmenorrhea may cause TLR binding, and subsequent activation of the pro-inflammatory cascade leading to increased secretion of mediators involved in apoptosis, haemostasis, inflammation and repair
Alterations in prostaglandin and cytokine expression in the endometrium of these women, combined with an altered microbiome may well contribute to ongoing activation of an innate immune response leading to dysregulation of the normal menstrual cycle associated with tissue remodelling
Summary
Cyclic tissue remodelling in the endometrium occurs under the influence of fluctuating levels of the ovarian steroid hormones estradiol and progesterone [4,5] (Figure 1). Steroid receptors for estrogens, progestins and androgens have been reported to fluctuate throughout the menstrual cycle. The ovarian steroid hormones modulate the ability of each to respond to the other and other hormone–dependent factors [6]. Both estrogen and progestin receptors peak during the second half of the proliferative phase of the cycle, and decline during the secretory phase of the cycle in response to progesterone, though to varying degrees for each isoform [7,8,9,10]. Androgen receptor expression decreases from the proliferative until the mid-secretory phase and is undetectable by the late secretory phase [11]
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