Lipopolysaccharide promotes early endometrial-peritoneal interactions in a mouse model of endometriosis

Keyama, Kaoru; Kato, Takeshi; Kadota, Yuri; Erdenebayar, Otgontsetseg; Kasai, Kana; Kawakita, Takako; Tani, Akio; Matsui, Shinji; Iwasa, Takeshi; Yoshida, Kanako; Murakami, Masahiko; Kuwahara, Akira; Matsuzaki, Takashi; Irahara, Minoru

doi:10.2152/jmi.66.70

Cited by 13 publications

(12 citation statements)

References 16 publications

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“…Our mouse model was created by implanting intrauterine tissue pieces and blood into the peritoneal cavity for mimicking the reflux of menstrual blood (23). Our study showed that LPS induced an inflammatory response in the peritoneal cavity, thereby promoting proliferation of endometriotic lesion (22).…”

Section: Discussionmentioning

confidence: 90%

“…We investigated the occurrence and proliferation of the inflammatory environment and endometriosis in the abdominal cavity. Azuma et al and we showed that intraperitoneal administration of lipopolysaccharide (LPS) promoted proliferation of endometriotic lesions in a model mouse of endometriosis (21,22). Our mouse model was created by implanting intrauterine tissue pieces and blood into the peritoneal cavity for mimicking the reflux of menstrual blood (23).…”

Section: Discussionmentioning

confidence: 90%

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Intraperitoneal administration of activin A promotes development of endometriotic lesions in a mouse model of endometriosis

et al. 2019

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 90%

Intraperitoneal administration of activin A promotes development of endometriotic lesions in a mouse model of endometriosis

et al. 2019

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“…An additive effect has been observed with the simultaneous treatment of macrophages with LPS and E2, which induced secretion of pro-inflammatory factors and proliferation of endometriotic cells (55). The above suggests a role of LPS in coordination with steroid hormones in the first stages of endometriosis development through induction of inflammatory responses and recruitment of neutrophils to endometriotic lesions, which in turn possibly participate in the release of angiogenic factors, unchaining a process of inflammatory angiogenesis (122). These observations have to be taken carefully since findings can be caused by an asymptomatic or subclinical vaginal infection or contamination with bacteria from cervicovaginal microbiota that contribute to bacterial contamination of analyzed samples (124).…”

Section: Contribution Of Inflammation Of Bacterial Origin To Endometrmentioning

confidence: 87%

“…Taking these results as antecedent, using a mouse model of endometriosis, it was demonstrated that simultaneous administration of blood (simulating menstrual reflux that reaches pelvic cavity during retrograde menstruation) with LPS in mice, which were previously injected with endometrial implants, induces the growth of endometriotic lesions and the production of TNF-α, IL-6, and MIP-2 in peritoneal fluid (122), which in turn is related with NF-κB expression (123). An additive effect has been observed with the simultaneous treatment of macrophages with LPS and E2, which induced secretion of pro-inflammatory factors and proliferation of endometriotic cells (55).…”

Section: Contribution Of Inflammation Of Bacterial Origin To Endometrmentioning

confidence: 97%

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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“…The bacterial contamination hypothesis suggests that microbial pathogens activate the immune response by binding with Toll‐like receptors . Lipopolysaccharide is a bacterial endotoxin and marker of inflammation found in the cell wall of Gram‐negative bacteria, which has been shown to promote the onset and progression of endometriosis lesions via binding with Toll‐like receptor 4 . Eight studies detected taxa belonging to the phylum Proteobacteria that were significantly increased in endometriosis cohorts .…”

Section: Discussionmentioning

confidence: 99%

Endometriosis and the microbiome: a systematic review

Leonardi

Hicks

El‐Assaad

et al. 2019

BJOG

116

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Background The aetiology and pathogenesis of endometriosis are still under investigation. There is evidence that there is a complex bidirectional interaction between endometriosis and the microbiome.Objective To systematically review the available literature on the endometriosis-microbiome interaction, with the aim of guiding future inquiries in this emerging area of endometriosis research.Search strategy MEDLINE, Embase, Scopus and Web of Science were searched through May 2019. A manual search of reference lists of relevant studies was also performed.Selection criteria Published and unpublished literature in any language describing a comparison of the microbiome state in mammalian hosts with and without endometriosis.Data collection and analysis Identified studies were screened and assessed independently by two authors. Data were extracted and compiled in a qualitative synthesis of the evidence.Main results Endometriosis appears to be associated with an increased presence of Proteobacteria, Enterobacteriaceae, Streptococcus spp. and Escherichia coli across various microbiome sites. The phylum Firmicutes and the genus Gardnerella also appear to have an association; however, this remains unclear.Conclusions The complex bidirectional relationship between the microbiome and endometriosis has begun to be characterised by the studies highlighted in this systematic review. Laboratory and clinical studies demonstrate that there are indeed differences in the microbiome composition of hosts with and without endometriosis.

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Lipopolysaccharide promotes early endometrial-peritoneal interactions in a mouse model of endometriosis

Cited by 13 publications

References 16 publications

Intraperitoneal administration of activin A promotes development of endometriotic lesions in a mouse model of endometriosis

Intraperitoneal administration of activin A promotes development of endometriotic lesions in a mouse model of endometriosis

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

Endometriosis and the microbiome: a systematic review

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