Villainous role of estrogen in macrophage-nerve interaction in endometriosis

Liang, Y. Daniel; Xie, Hongyu; Wu, Jinjie; Liu, Duo; Yao, Shuzhong

doi:10.1186/s12958-018-0441-z

Cited by 57 publications

(49 citation statements)

References 96 publications

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“…Why a transplanted or congenital ectopic endometrium develops into endometriosis is the source of much research. The causes of this development include research on the role of estrogen and estrogen receptors (ERs), the estrogen-dependent physiologic and molecular changes [71], the local levels of estrogen [71,72], the role of estrogen in macrophage-nerve interaction [72], the effects of environmental toxicants on estrogen signaling [73], and the intracellular estrogen production related to aromatase activity. In addition, the normal control of cyclic estrogen and progesterone requires activation and crosstalk of cAMP and progesterone mediated signaling pathways [74].…”

Section: Behind the Origins Of Endometriosismentioning

confidence: 99%

The Pathogenesis of Endometriosis: Molecular and Cell Biology Insights

Laganà

Garzon

Götte

et al. 2019

IJMS

336

265

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The etiopathogenesis of endometriosis is a multifactorial process resulting in a heterogeneous disease. Considering that endometriosis etiology and pathogenesis are still far from being fully elucidated, the current review aims to offer a comprehensive summary of the available evidence. We performed a narrative review synthesizing the findings of the English literature retrieved from computerized databases from inception to June 2019, using the Medical Subject Headings (MeSH) unique ID term “Endometriosis” (ID:D004715) with “Etiology” (ID:Q000209), “Immunology” (ID:Q000276), “Genetics” (ID:D005823) and “Epigenesis, Genetic” (ID:D044127). Endometriosis may origin from Müllerian or non-Müllerian stem cells including those from the endometrial basal layer, Müllerian remnants, bone marrow, or the peritoneum. The innate ability of endometrial stem cells to regenerate cyclically seems to play a key role, as well as the dysregulated hormonal pathways. The presence of such cells in the peritoneal cavity and what leads to the development of endometriosis is a complex process with a large number of interconnected factors, potentially both inherited and acquired. Genetic predisposition is complex and related to the combined action of several genes with limited influence. The epigenetic mechanisms control many of the processes involved in the immunologic, immunohistochemical, histological, and biological aberrations that characterize the eutopic and ectopic endometrium in affected patients. However, what triggers such alterations is not clear and may be both genetically and epigenetically inherited, or it may be acquired by the particular combination of several elements such as the persistent peritoneal menstrual reflux as well as exogenous factors. The heterogeneity of endometriosis and the different contexts in which it develops suggest that a single etiopathogenetic model is not sufficient to explain its complex pathobiology.

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Section: Behind the Origins Of Endometriosismentioning

confidence: 99%

The Pathogenesis of Endometriosis: Molecular and Cell Biology Insights

Laganà

Garzon

Götte

et al. 2019

IJMS

336

265

View full text Add to dashboard Cite

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“…Endometriosis lesions aberrantly express a number of steroidogenic enzymes including aromatase and 17β-hydroxysteriod dehydrogenase (17β-HSD), this results in increased synthesis and decreased metabolism of estrogen (27)(28)(29) such that local levels remain high. Estrogen signaling modulates a large number of down-stream disease processes within endometriosis lesions, which are reviewed in Yilmaz and Bulun (30), Liang et al (31), and Rizner (32). Immune cell dysfunction is also intrinsically linked to the pathophysiology of endometriosis.…”

Section: Etiology and Natural Historymentioning

confidence: 99%

Endometriosis-Associated Macrophages: Origin, Phenotype, and Function

2020

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Endometriosis is a complex, heterogeneous, chronic inflammatory condition impacting ∼176 million women worldwide. It is associated with chronic pelvic pain, infertility, and fatigue, and has a substantial impact on health-related quality of life. Endometriosis is defined by the growth of endometrial-like tissue outside the uterus, typically on the lining of the pelvic cavity and ovaries (known as "lesions"). Macrophages are complex cells at the center of this enigmatic condition; they are critical for the growth, development, vascularization, and innervation of lesions as well as generation of pain symptoms. In health, tissue-resident macrophages are seeded during early embryonic life are vital for development and homeostasis of tissues. In the adult, under inflammatory challenge, monocytes are recruited from the blood and differentiate into macrophages in tissues where they fulfill functions, such as fighting infection and repairing wounds. The interplay between tissue-resident and recruited macrophages is now at the forefront of macrophage research due to their differential roles in inflammatory disorders. In some cancers, tumor-associated macrophages (TAMs) are comprised of tissue-resident macrophages and recruited inflammatory monocytes that differentiate into macrophages within the tumor. These macrophages of different origins play differential roles in disease progression. Herein, we review the complexities of macrophage dynamics in health and disease and explore the paradigm that under disease-modified conditions, macrophages that normally maintain homeostasis become modified such that they promote disease. We also interrogate the evidence to support the existence of multiple phenotypic populations and origins of macrophages in endometriosis and how this could be exploited for therapy.

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“…Many reports have indicated that the process of endometriosis is related to a dysregulation of the host immune and some researchers even consider EMS to be an autoimmune disorder [5–12]. On one hand, some studies have been focused on downregulation of anti-endometrial implants cells, such as NK cells, CD4 + /CD8 + T cells, B cells and so on [5–8], on the other hand, some studies demonstrated that increased immunosuppressive cells could promote the progression of endometriosis, such as Tregs (regulatory T cells), TH2 (T helper) cells and even MDSCs (myeloid derived suppressor cells), which have been suggested recently to promote the implantation of endometrial tissue [13, 14]. All these evidences pointed to the fact that the impaired immune response exists in endometriosis.…”

Section: Introductionmentioning

confidence: 99%

CD4+/CD8+ mucosa-associated invariant T cells foster the development of endometriosis: a pilot study

et al. 2019

Reprod Biol Endocrinol

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Background Immune dysregulation is one of the mechanisms to promote endometriosis (EMS). Various T cell subpopulations have been reported to play different roles in the development of EMS. The mucosa-associated invariant T cell (MAIT) is an important T cell subset in the pathogenesis of various autoimmune diseases. Evidence has indicated that there are three functionally distinct MAIT subsets: CD4+, CD8+ and CD4/CD8−/− (double negative, DN) MAIT cells. Till now, the associations between endometriosis and MAIT have not been studied. Our research investigates different MAIT subpopulations in peripheral blood (PB) and peritoneal fluid (PF) from EMS patients. Methods Thirty-two EMS patients and eighteen controls were included. PB and PF were collected. Tests of cytokines in plasma and PF were performed by ELISA kit. Characterisations of MAIT were done by flow cytometry. MAIT cells have been defined as CD3 + CD161 + Vα7.2+ cells. Based on CD4 and CD8 expression, they were divided into CD8+MAIT, CD4+MAIT and DN MAIT. Results Enrichments of MAIT cells, especially CD4 and CD8 MAIT subsets were found. Moreover, CD8 MAIT cells had a high activation in the EMS group. EMS patients produced higher level of IL-8/12/17 as compared to these from controls. On the contrary, control patients exhibited an impressive upregulation of DN MAIT cells, however, these DN MAIT cells from controls showed a higher expression of PD-1. Lastly, we performed the relevance analysis, and discovered that the accumulation of PB MAIT cells positively correlated with an elevated level of serum CA125 production in EMS group. Conclusion These results suggest that different MAIT subsets play distinct roles in the progression of endometriosis.

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Villainous role of estrogen in macrophage-nerve interaction in endometriosis

Cited by 57 publications

References 96 publications

The Pathogenesis of Endometriosis: Molecular and Cell Biology Insights

The Pathogenesis of Endometriosis: Molecular and Cell Biology Insights

Endometriosis-Associated Macrophages: Origin, Phenotype, and Function

CD4+/CD8+ mucosa-associated invariant T cells foster the development of endometriosis: a pilot study

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