Pathogenesis of endometriosis: Look no further than John Sampson

Yovich, John L.; Rowlands, Philip; Lingham, Sunthra; Sillender, Mark; Srinivasan, Shanthi

doi:10.1016/j.rbmo.2019.10.007

Cited by 52 publications

(41 citation statements)

References 11 publications

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“…Endometriosis is a multifactorial disease, and its aetiology and pathogenesis are still ill-established. One of the most widely accepted theories on the origin of ectopic endometrial tissues is “Retrograde Menstruation”, which refers to the reflux of menstrual debris with viable endometrial cells via the fallopian tubes into the pelvic cavity [ 1 , 15 , 16 ]. Once there, cells in the endometrial deposits must adhere to peritoneal surfaces and proliferate in order to develop into invasive lesions ( Figure 1 ) [ 17 , 18 ].…”

Section: Endometriosismentioning

confidence: 99%

Intricate Connections between the Microbiota and Endometriosis

Jiang

Yong

Allaire

et al. 2021

IJMS

103

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Imbalances in gut and reproductive tract microbiota composition, known as dysbiosis, disrupt normal immune function, leading to the elevation of proinflammatory cytokines, compromised immunosurveillance and altered immune cell profiles, all of which may contribute to the pathogenesis of endometriosis. Over time, this immune dysregulation can progress into a chronic state of inflammation, creating an environment conducive to increased adhesion and angiogenesis, which may drive the vicious cycle of endometriosis onset and progression. Recent studies have demonstrated both the ability of endometriosis to induce microbiota changes, and the ability of antibiotics to treat endometriosis. Endometriotic microbiotas have been consistently associated with diminished Lactobacillus dominance, as well as the elevated abundance of bacterial vaginosis-related bacteria and other opportunistic pathogens. Possible explanations for the implications of dysbiosis in endometriosis include the Bacterial Contamination Theory and immune activation, cytokine-impaired gut function, altered estrogen metabolism and signaling, and aberrant progenitor and stem-cell homeostasis. Although preliminary, antibiotic and probiotic treatments have demonstrated efficacy in treating endometriosis, and female reproductive tract (FRT) microbiota sampling has successfully predicted disease risk and stage. Future research should aim to characterize the “core” upper FRT microbiota and elucidate mechanisms behind the relationship between the microbiota and endometriosis.

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Section: Endometriosismentioning

confidence: 99%

Intricate Connections between the Microbiota and Endometriosis

Jiang

Yong

Allaire

et al. 2021

IJMS

103

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“…In addition to the implantation hypothesis [ 5 ] or metaplasia theory [ 23 ], alternative hypotheses such as the genetic/epigenetic theory [ 26 ], circulating stem/progenitor cells [ 27 ], repeated tissue injury and repair (ReTIAR) caused by uterine hyperperistalsis [ 28 ], and a fetal [ 29 ] or adolescent [ 30 ] origin were also suggested. Many arguments were put forward to criticize the implantation hypothesis such as the occurrence of extra-pelvic endometriosis [ 31 ]; however, as clearly shown in a recent review [ 32 ], Sampson already mentioned the vascular spread. In addition to this recent reappraisal of Sampson’s work, Shakiba et al [ 33 ] showed that patients with hysterectomy combined with laparoscopy experience a dramatically lower recurrence rate of 96.0%, 91.7%, and 91.7% compared to laparoscopy alone with a recurrence rate of 79.0%, 53.3%, and 44.6% after two, five, and seven years, respectively.…”

Section: Endometriosismentioning

confidence: 99%

“…The implications for the clinicians are obvious; endometriosis should be better prevented by the use of mechanical barriers such as for example levonorgestrel-releasing intrauterine devices (LNG-IUDs), which are also helpful in reduction of recurrence [ 100 ]. Furthermore, the total ablation of the endometrium in women without the wish to conceive should be used more often [ 32 ]. Furthermore, reduction of repetitive stress, reduction of microtrauma, and prevention of peritoneal inflammation may be useful [ 26 ].…”

Section: Emt In Endometriosis—when Does It Happen?mentioning

confidence: 99%

Epithelial–Mesenchymal Transition in Endometriosis—When Does It Happen?

Konrad

Dietze

Riaz

et al. 2020

JCM

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Epithelial–mesenchymal transition (EMT) is an important process of cell remodeling characterized by the gradual loss of the epithelial phenotype and progressive gain of a mesenchymal phenotype. EMT is not an all-or-nothing process, but instead a transition of epithelial to mesenchymal cells with intermediate cell states. Recently, EMT was described in endometriosis, and many EMT-specific pathways like Twist, Snail, Slug, Zinc finger E-box-binding homeobox 1/2 (ZEB1/2), E/N-cadherin, keratins, and claudins are involved. However, as pointed out in this review, a comparison of the eutopic endometrium of women with and without endometriosis yielded only subtle changes of these EMT markers. Furthermore, only very few alterations in cell–cell contacts could be found but without changes in the epithelial phenotype. This suggests only a partial EMT which is not a prerequisite for the detachment of endometrial cells and, thus, not critical for the first step(s) in the pathogenesis of endometriosis. In contrast, the majority of changes in the EMT-related marker expression were found in the ectopic endometrium, especially in the three endometriotic entities, ovarian, peritoneal, and deep infiltrating endometriosis (DIE), compared with the eutopic endometrium. In this review, we examine the most important EMT pathways described in endometriosis and propose that partial EMT might result from the interaction of endometrial implants with their surrounding microenvironment.

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“…Severe adversity induced psychological stresses, such as bereavement, in early life have been reported to be associated with accelerated development of certain malignancies [42,43]. Although such data are lacking for endometriosis, one study has reported that childhood physical abuse is associated with risk of developing endometriosis [17], suggesting that ELAaccelerated lesional progression is biologically plausible, especially given that retrograde menstruation is nearly universal and is likely the cause for endometriosis [44]. Thus, a recent proposition that trauma, physical or otherwise, increases the risk of endometriosis [45] may have some merits.…”

Section: Discussionmentioning

confidence: 99%

Early maternal separation accelerates the progression of endometriosis in adult mice

Long

Liu

Guo

2020

Reprod Biol Endocrinol

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Background A large body of research highlights the importance of early-life environmental impact on the health outcome in adulthood. However, whether early-life adversity (ELA) has any impact on the development of endometriosis is completely unclear. In this study, we tested the hypothesis that ELA, as manifested by neonatal separation, can accelerate the progression of endometriosis in mouse through activation of the adrenergic receptor β2 (ADRB2) signaling pathway, leading to increased angiogenesis and progression of endometriotic lesions. Methods Eight female Balb/C mice, in late pregnancy, were used used for this study, which later gave birth to 22 female newborn pubs. Eleven additional female Balb/C mice were also used as donors of uterine tissues. The 22 newborn pubs were randomly divided into 2 equal-sized groups, maternal separation (MS) and no separation (NS). Pubs in the MS group were separated from their dams for 3 h/day from postnatal day (PND) 1 to 21, while those in the NS control remained in the home cage with their dams. In adulthood (8-week old), 3 mice in each group were randomly selected to undergo a battery of behavior tests. The remaining 8 mice in each group were induced with endometriosis by intraperitoneal injection of uterine fragments from donor mice. Four weeks after the induction, all mice were sacrificed and their endometriotic lesions were excised for quantification and then prepared for immunohistochemistry analysis. Results We confirmed that MS during infancy resulted in anxiety and depression-like behaviors as previously reported. We also found that in MS mice the lesion weight was increased by over 2 folds and generalized hyperalgesia was also significantly increased as compared with NS mice. Immunostaining analysis demonstrated that MS accelerated the development of endometriosis likely through decreased dopamine receptor D2 (DRD2) expression and activation of the ADRB2/cAMP-response element binding protein (CREB) signaling pathway, leading to increased angiogenesis and progression of endometriotic lesions. Conclusions Exposure of female mouse pups to ELA such as MS during their infancy period accelerates the progression of endometriosis, possibly through altered neuronal wiring and hyperactivity of the hypothalamic-pituitary-adrenal axis.

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Pathogenesis of endometriosis: Look no further than John Sampson

Cited by 52 publications

References 11 publications

Intricate Connections between the Microbiota and Endometriosis

Intricate Connections between the Microbiota and Endometriosis

Epithelial–Mesenchymal Transition in Endometriosis—When Does It Happen?

Early maternal separation accelerates the progression of endometriosis in adult mice

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