Hypothetical roadmap towards endometriosis: prenatal endocrine-disrupting chemical pollutant exposure, anogenital distance, gut-genital microbiota and subclinical infections (original) (raw)
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Endometriosis and the human microbioma
JOURNAL OF CLINICAL SEXOLOGY
The dysbiosis of the intestinal microbiome is associated with various diseases. It is important to understand the factors that influence the intestinal microbiome and the microbiome regulation strategies to increase therapeutic responses. Endometriosis affects about 10% of women of childbearing age. Among those affected by endometriosis, up to 50% of them suffer from chronic pelvic pain and / or infertility. Endometriosis is characterized by inflammation and oestrogen dependence. Endometriosis is a condition that affects fertility, creates a state of "congestion" with an excessive growth of the endometrial tissue in many other areas of the body. The microbiota plays a role in the occurrence of endometriosis by affecting the epigenetic, immunological and / or biochemical functions of the host. Intestinal bacteria are involved in the oestrogen metabolism. The oestrogen-microbiome link (or the stroboloma) helps explain where the excess oestrogen comes from. Endometriosis appears to be associated with the increased presence of Proteobacteria, Enterobacteriaceae, Streptococcus spp. and Escherichia coli in various areas occupied by the microbiome. Further studies are needed to analyse the association between endometriosis and microbiota. Endometriosis is influenced by diet.
Journal of Pure and Applied Microbiology, 2021
Currently, unlike in the past, the endometrial cavity is not considered to be sterile. The endometrium is supposed to be dominated by Lactobacilli, but also their deficiency can be found in the reproductive tract of asymptomatic healthy women. Sometimes the endometrial microbiome is dominated by various pathological microorganisms, and this can lead to various conditions as chronic endometritis, chorioamnionitis and preterm birth. Their presence causes uterine inflammation and infection, release of pro-inflammatory molecules, uterine contractions, disruption of cervical barrier, premature rupture of membranes. Uterine dysbiosis is associated with recurrent implantation failure and recurrent miscarriages. As the microbiome is important for maintaining immunological homeostasis at the level of gastrointestinal tract Lactobacilli may play a similar function at the level of uterus. The lactobacillus-dominated uterine microbiome is of great importance for maintaining a hostile uterine mi...
Environmental factors and endometriosis
Revista da Associação Médica Brasileira (1992)
Endometriosis represents a common gynecological condition affecting 5%-15% of childbearing age women and up to 3% 5% of post-menopausal women. This disease is defined by the presence of stromal and/or endometrial glandular epithelium implants in extra-uterine locations possibly compromising several sites. Humans and animals are daily exposed to chemical pollutants that could adversely influence physiological processes and potentially cause diseases, including endometriosis. In this review, the authors aimed at settling the influence of environmental and dietary factors on endometriosis pathogenesis. The mechanism by which dioxin and its similes (TCDD/PCBs) act changing the endometrial physiology remains uncertain and is speculative due to the difficulty in assessing the exposure over intrauterine life, childhood and adulthood and its actual consequences, in addition to the limitations to its in vitro reproducibility. We need to better understand the mechanism of action of these envi...
Microbial dysbiosis and disease pathogenesis of endometriosis, could there be a link?
Endometriosis is an estrogen-dependent inflammatory condition in women that is characterised by the ectopic growth of endometrial glands and stroma outside of the uterine cavity. Although there exists many theories for the pathogenesis of endometriosis, none has been successively confirmed as a direct cause for disease development. The human body comprises a diverse microflora across all tissues that can have fundamental roles in health and disease. The microbial flora in a healthy individual can vary remarkably between anatomical sites due to the physical and chemical properties of specific tissues. This includes the female reproductive tract, notably the vagina, which harbors a microbiota dominated by Lactobacilli species. In addition, a core unique microbiome has been defined for the endometrium that also includes Lactobacilli spp. In this review we examine the possibility that endometriosis could result from microbial dysbiosis, whereby significant changes to the natural microflora within the endometrium could reduce mucosal immune regulation in this tissue with concomitant expansion of pathogenic bacteria that trigger local tissue inflammation that could perpetuate the development of endometrial disease.
Environment and Endometriosis: a toxic relationship
Endometriosis is a common, benign, estrogen-dependent gynecological disease that represents one of the main causes of hospitalization in industrialized countries. It is well established that a large amount of natural and man-made chemicals are present in the environment and both humans and animals are exposed to them. Dioxin and dioxin-like compounds have long biological half-life, can accumulate within the organism and could negatively affect several physiological processes. The purpose of this review is to provide an overview of the possible relationship between these chemicals and the pathogenesis of endometriosis.
In utero exposures and the incidence of endometriosis
Fertility and Sterility, 2004
Objective: To investigate the relation between the fetal environment and endometriosis. Design: Prospective cohort study. Setting: Nurses' Health Study II with 10 years of follow-up. Participant(s): Eighty-four thousand, four hundred forty-six women aged 25-42 who had never been diagnosed with endometriosis, infertility, or cancer at baseline in 1989. Main Outcome Measure(s): Incidence of laparoscopically confirmed endometriosis according to birthweight, prematurity, multiple gestation, diethylstilbestrol (DES) exposure, and having been breastfed. Result(s): During 566,250 woman-years of follow-up, 1,226 cases of laparoscopically-confirmed endometriosis were reported among women with no past infertility. After adjusting for age, calendar time, parity, race, and body mass index at age 18, we observed a linear increase in the incidence rate with decreasing birthweight (rate ratio [RR] ϭ 1.3 for birthweight Ͻ5.5 pounds versus 7.0 -8.4 pounds, 95% confidence interval [CI] ϭ 1.0 -1.8, P value, test for trend ϭ .01). In addition, women who were born as one of a multiple gestation (i.e., twins or greater number) were at increased risk even after controlling for birthweight (RR ϭ 1.7, CI ϭ 1.2-2.5). The rate of endometriosis was also 80% greater among women exposed to diethylstilbestrol in utero (RR ϭ 1.8, CI ϭ 1.2-2.8). Neither premature delivery nor having been breastfed were associated with the incidence of endometriosis. None of these effect estimates were modified by infertility status at the time of endometriosis diagnosis.
Menstrual Effluent Provides a Novel Diagnostic Window on the Pathogenesis of Endometriosis
Frontiers in Reproductive Health, 2020
Endometriosis is a chronic inflammatory disorder characterized by the presence of endometrial-like tissue growing outside of the uterus. Although the cause is unknown, retrograde menstruation leads to deposition of endometrial cells into the peritoneal cavity. Lack of disease recognition and long diagnostic delays (6-10 years) lead to substantial personal, social and financial burdens, as well as delayed treatment. A non-invasive diagnostic for endometriosis is a major unmet clinical need. Here, we assessed whether differences in menstrual effluent-derived stromal fibroblast cells (ME-SFCs) from women with and without endometriosis provide the basis for a non-invasive diagnostic for endometriosis. In addition, we investigated whether treatment of control ME-SFCs with inflammatory cytokines (TNF and IL-1β) could induce an endometriosis-like phenotype. ME-SFCs from laparoscopically diagnosed endometriosis patients exhibit reduced decidualization capacity, measured by IGFBP1 production after exposure to cAMP. A receiver operating characteristic (ROC) curve developed using decidualization data from controls and endometriosis subjects yielded an area under the curve of 0.92. In addition, a significant reduction in ALDH1A1 gene expression and increased podoplanin surface expression were also observed in endometriosis ME-SFCs when compared to control ME-SFCs. These endometriosis-like phenotypes can be reproduced in control ME-SFCs by exposure to inflammatory cytokines (TNF and IL-1β) and are associated with increased cell migration. These results are consistent with the hypothesis that chronic intrauterine inflammation influences the development of endometriosis lesions following retrograde menstruation. In conclusion, the analysis of ME-SFCs can provide an accurate, rapid, and non-invasive diagnostic for endometriosis and insight into disease pathogenesis.
Environmental Contaminants and Dietary Factors in Endometriosis
Annals of the New York Academy of Sciences, 2002
Endometriosis is an estrogen-dependent disease characterized by the presence of endometrial glands and stroma outside the uterine cavity. The etiology of this disease remains elusive, but is clearly influenced by genetic, immune, and endocrine factors. Exposure to environmental contaminants has recently been added to the list of potential factors that contribute to the pathogenesis of endometriosis. The objective of this paper is to review the weight of the evidence from hospital-based case-control studies and animal experiments for an association between exposure to environmental contaminants and endometriosis.
2019
Background: The genetic-epigenetic theory postulates that endometriosis is triggered by a cumulative set of genetic-epigenetic (GE) incidents. Pelvic and upper genital tract infection might induce GE incidents and thus play a role in the pathogenesis of endometriosis. Thus, this article aims to review the association of endometriosis with upper genital tract and pelvic infections. Methods: Pubmed, Scopus and Google Scholar were searched for 'endometriosis AND (infection OR PID OR bacteria OR viruses OR microbiome OR microbiota)', for 'reproductive microbiome' and for 'reproductive microbiome AND endometriosis', respectively. All 384 articles, the first 120 'best match' articles in PubMed for 'reproductive microbiome' and the first 160 hits in Google Scholar for 'reproductive microbiome AND endomytriosis' were hand searched for data describing an association between endometriosis and bacterial, viral or other infections. All 31 articles found were included in this manuscript. Results: Women with endometriosis have a significantly increased risk of lower genital tract infection, chronic endometritis, severe PID and surgical site infections after hysterectomy. They have more colony forming units of Gardnerella, Streptococcus, Enterococci and Escherichia coli in the endometrium. In the cervix Atopobium is absent, but Gardnerella, Streptococcus, Escherichia, Shigella, and Ureoplasma are increased. They have higher concentrations of Escherichia Coli and higher concentrations of bacterial endotoxins in menstrual blood. A Shigella/Escherichia dominant stool microbiome is more frequent. The peritoneal fluid of women with endometriosis contains higher concentrations of bacterial endotoxins and an increased incidence of mollicutes and of HPV viruses. Endometriosis lesions have a specific bacterial colonisation with more frequently mollicutes (54%) and both high and medium-risk HPV infections (11%). They contain DNA with 96% homology with Shigella. In mice transplanted endometrium changes the gut microbiome while the gut microbiome influences the growth of these endometriosis lesions. Conclusions: Endometriosis is associated with more upper genital tract and peritoneal infections. These infections might be co-factors causing GE incidents and influencing endometriosis growth.