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Gut microbiome and its products promote endometriosis in animal model

Gut microbiome and its products promote endometriosis in animal model
Generation of microbiota-depleted mice using antibiotics. A Schematic of experimental timeline and procedures. B Quantification of relative abundances of Bacteroidetes, Firmicutes, and Gamma-proteobacteria in feces from vehicle and Microbiota-depleted (MD) mice. C-D Wet weights of C spleen and D caecum in indicated treatment groups at a sacrifice. E The number of Peyer’s patches from indicated treatment groups. F Representative images of Hematoxylin and Eosin-stained uterine cross-sections from the indicated treatment groups. LE, Luminal Epithelium; GE, Glandular Epithelium; S, Stroma. Yellow arrows indicate the gland. G-H Mouse G body weight and H water consumption at indicated time points in vehicle and MD mice. I-J Relative level of I 17β-Estradiol in serum and J IL-1β in peritoneal fluid of indicated treatment groups. Data are presented as mean ± SE (n = 5 mice per group). **P < 0.01, ***P < 0.001, and ns, non-significant. Credit: Cell Death Discovery (2023). DOI: 10.1038/s41420-023-01309-0

About 196 million women worldwide suffer from endometriosis, a condition that typically causes pelvic pain and infertility. Endometriosis develops when lining inside the womb grows attached to surrounding tissues, such as the intestine or the membrane lining the abdominal cavity, causing bleeding, pain and other symptoms. Despite decades of research, little is known about the factors that contribute to the development of endometriosis.

Evidence suggests that the , a community of microorganisms living inside the body, is altered in women with endometriosis. In this study published in the journal Cell Death & Discovery, researchers at Baylor College of Medicine discovered that an altered gut microbiome plays a pivotal role in endometriosis disease progression in an animal model.

"To investigate the role of the microbiome in endometriosis we first implemented a novel mouse model of the condition in which we eliminated the microbiome using antibiotics," said lead author Dr. Rama Kommagani, associate professor in the Departments of Pathology and Immunology and of Molecular Virology and Microbiology at Baylor.

The researchers found that mice lacking gut microbiome had smaller endometriotic lesions than mice with a microbiome. Furthermore, when gut microbiome-free mice received from mice with endometriosis, the lesions grew as large as those in mice retaining their microbiome. These findings suggest that altered gut bacteria drive disease progression. On the other hand, the uterine microbiome did not seem to affect disease progression.

The team also discovered a novel signature of microbiome-derived metabolites, products produced by the microbes, that were significantly altered in feces of mice with endometriosis. Supporting the role of microbiome metabolites in disease progression, Kommagani and his colleagues found that treatment of endometriotic cells and mice with the called quinic acid significantly enhanced the cellular proliferation and endometriotic lesion growth, respectively.

The findings suggest that certain microbiome communities and/or their metabolites can contribute to endometriosis progression and that modifying the composition of these communities could help control the condition in . "We are currently investigating this possibility," Kommagani said.

The findings also suggested that studying microbiome metabolites in human stool samples could be used as a diagnostic tool. "Endometriosis is typically diagnosed with ultrasound, and an invasive procedure is necessary to characterize the lesion well," Kommagani said. "We are investigating whether microbiome metabolites in human stool samples could be a useful diagnostic tool and also whether some of these metabolites could be used as a treatment strategy."

Women with also tend to have bowel issues, such as colitis or inflammatory bowel syndrome. "We are interested in determining whether changes in the could affect bowel conditions and the possibility of controlling them by modifying the microbiome or with their metabolites," Kommagani said.

More information: Sangappa B. Chadchan et al, Gut microbiota and microbiota-derived metabolites promotes endometriosis, Cell Death Discovery (2023). DOI: 10.1038/s41420-023-01309-0

Citation: Gut microbiome and its products promote endometriosis in animal model (2023, January 25) retrieved 28 February 2024 from
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