Mast cells in endometriosis: guilty or innocent bystanders?

Kirchhoff, Dennis; Kaulfuß, Stefan; Fuhrmann, Ulrike; Maurer, Marcus; Zollner, Thomas M.

doi:10.1517/14728222.2012.661415

Cited by 32 publications

(31 citation statements)

References 39 publications

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“…These findings agree with the trend revealed by the preliminary analysis of cytocentrifuged samples stained with TB reported in Table 2. Of note the density of tryptase-positive cells in the endometriotic lesions ( Supplementary Figure S1 and Supplementary Table S2) is comparabe with those reported in the literature (Konno et al, 2003;Kempuraj et al, 2004;Sugamata et al, 2005;Anaf et al, 2006;Kirchhoff et al, 2012;Paula et al, 2015).…”

Section: Blood Cell Counts and Peritoneal Fluid Characterization Of Tsupporting

confidence: 77%

“…However, the pathogenesis of this disease is still unknown, so that in several cases the available treatments for symptoms are ineffective (Zito et al, 2014). Increasing evidence supports an involvement of MC either in the inflammatory process of EMS (Kirchhoff et al, 2012) and infertility (Meineke et al, 2000;Weidinger et al, 2003Weidinger et al, , 2005Roaiah et al, 2007;Haidl et al, 2011;Menzies et al, 2011). MC are normal constituents of the human myometrium and endometrium and are present in the female genital tract (Sivridis et al, 2001;Hunt and Lynn, 2002).…”

Section: Discussionmentioning

confidence: 99%

“…However, increasing evidence supports the involvement of MC also in the inflammatory process of EMS. High numbers of degranulated MC have been found in endometriotic lesions (Konno et al, 2003;Kempuraj et al, 2004;Sugamata et al, 2005;Anaf et al, 2006;Kirchhoff et al, 2012;Paula et al, 2015). Of note, this was not the case at unaffected sites of the peritoneum or eutopic endometrial tissue from EMS patients or healthy controls.…”

Section: Introductionmentioning

confidence: 92%

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Mast Cells in Peritoneal Fluid From Women With Endometriosis and Their Possible Role in Modulating Sperm Function

et al. 2020

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Endometriosis is a local pelvic inflammatory process, frequently associated with infertility, with altered function of immune-related cells in the peritoneal environment. Mast cells are known to be key players of the immune system and have been recently involved in endometriosis and in infertility, with their mediators directly suppressing sperm motility. In this study, we evaluated the mast cell population and their mediators in the peritoneal fluid of infertile patients with endometriosis and their impact on human sperm motility. Peritoneal fluids, collected by laparoscopy from 11 infertile patients with endometriosis and 9 fertile controls were evaluated for the presence of mast cells, tryptase levels and their effect on sperm motility. Furthermore, an in vitro model of mast cells-sperm interaction in peritoneal fluid was set up, using LAD2 cell line as a mast cell model, and analyzed from a functional as well as a morphological point of view. Mast cell peritoneal fluid population and its main mediator, tryptase, is more represented in endometriosis confirming an involvement of these cells in this disease. Anyway it appears unlikely that tryptase enriched peritoneal fluid, which fails to inhibit sperm motility, could contribute to endometriosis associated infertility. Despite of this, sperm interaction with the mast cell surface (LAD2) induced a significantly mast cell-degranulation response in the peritoneal fluid from endometriosis which could directly modulate sperm function other than motility. This evidence lead us to suppose that there is, between these elements, an interrelationship which deserves further studies.

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Section: Blood Cell Counts and Peritoneal Fluid Characterization Of Tsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 92%

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Mast Cells in Peritoneal Fluid From Women With Endometriosis and Their Possible Role in Modulating Sperm Function

et al. 2020

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“…Mast cells are another group of leukocytes that are involved in endometriosis by modulating the recruitment, survival, development, phenotype, or function of other immune cells involved in endometriosis pathology, including macrophages, granulocytes, dendritic cells, and T and B cells (79). High numbers of degranulated mast cells have been found in endometriotic lesions, mainly of deep infiltrating type, but not in non-affected areas from peritoneum or eutopic endometrium of patients, indicating that a reaction of hypersensitivity is strongly associated to endometriosis (80); released mediators include TNF-α, IL-8, MCP-1, RANTES, and stem cell factor (SCF) (81).…”

Section: Alteration Of Immune Cell Functionmentioning

confidence: 99%

Regulation of Inflammation Pathways and Inflammasome by Sex Steroid Hormones in Endometriosis

et al. 2020

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Endometriosis is a gynecological disorder characterized by the growth of endometrial tissue (glands and stroma) outside the uterus, mainly in the peritoneal cavity, ovaries, and intestines. This condition shows estrogen dependency and progesterone resistance, and it has been associated with chronic inflammation, severe pain, and infertility, which negatively affect the quality of life in reproductive women. The molecular mechanisms involved in the pathogenesis of endometriosis are not completely understood; however, inflammation plays a key role in the pathophysiology of the disease, mainly by altering the function of immune cells (macrophages, natural killer, and T cells) and increasing levels of pro-inflammatory mediators in the peritoneal cavity, endometrium, and blood. These immune alterations inhibit apoptotic pathways and promote adhesion and proliferation of endometriotic cells, as well as angiogenesis and neurogenesis in endometriotic lesions. It has been demonstrated that hormonal alterations in endometriosis are related to the inflammatory unbalance in this disease. Particularly, steroid hormones (mainly estradiol) promote the expression and release of pro-inflammatory factors. Excessive inflammation in endometriosis contributes to changes of hormonal regulation by modulating sex steroid receptors expression and increasing aromatase activity. In addition, dysregulation of the inflammasome pathway, mediated by an alteration of cellular responses to steroid hormones, participates in disease progression through preventing cell death, promoting adhesion, invasion, and cell proliferation. Furthermore, inflammation is involved in endometriosis-associated infertility, which alters endometrium receptivity by impairing biochemical responses and decidualization. The purpose of this review is to present current research about the role of inflammasome in the pathogenesis of endometriosis as well as the molecular role of sex hormones in the inflammatory responses in endometriosis.

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“…Endometriosis is a common cause of pelvic pain, possibly by regulating the recruitment of their own unique neural supplies through neurogenesis (7). Although the precise reason for the endometriosis-associated increase in neurogenesis is unknown, there is evidence of a closer proximity between mast cells and nerve fibers, demonstrating that mast cells are able to contribute to the development of pain (5,8).…”

Section: Innate Immunity and Inflammation In Endometriosismentioning

confidence: 99%

Pathogenesis of endometriosis: The role of initial infection and subsequent sterile inflammation (Review)

Kobayashi

Higashiura

Shinmoto

et al. 2013

Molecular Medicine Reports

109

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Abstract. Endometriosis is a common type of chronic inflammatory disease with an immunological background. In this review, we aimed to explore the contemporary literature on the infection and sterile inflammation that support the pathogenesis of endometriosis. This article reviews the English-language literature on inflammatory, environmental, immunological and oxidative factors associated with endometriosis in an effort to identify factors that cause a predisposition to endometriosis. Intrauterine microbes may be critical for the initiation of endometriosis; the initial activation of pathogen recognition receptors by microbial stimuli results in the activation of proinflammatory pathways and innate immunity. In addition to their response to various exogenous pathogen-associated molecular patterns, Toll-like receptors (TLRs) also recognize a wide range of endogenous danger-associated molecular patterns (DAMPs). The increased expression levels of DAMPs may be involved in the subsequent process of nuclear transcription factor-κB-dependent sterile inflammation. Oxidative stress, secondary to the influx of iron during retrograde menstruation, is involved in the progression of endometriosis. DAMP-mediated danger signals and oxidative stress are bidirectional during sterile inflammation (danger signal spiral). This review supports the hypothesis that there are at least two distinct phases of endometriosis development: The initial wave of TLR activation in modulating innate immune responses would be followed by the second big wave of sterile inflammation.

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Mast cells in endometriosis: guilty or innocent bystanders?

Cited by 32 publications

References 39 publications

Mast Cells in Peritoneal Fluid From Women With Endometriosis and Their Possible Role in Modulating Sperm Function

Mast Cells in Peritoneal Fluid From Women With Endometriosis and Their Possible Role in Modulating Sperm Function

Regulation of Inflammation Pathways and Inflammasome by Sex Steroid Hormones in Endometriosis

Pathogenesis of endometriosis: The role of initial infection and subsequent sterile inflammation (Review)

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