Estrobolome dysregulation is associated with altered immunometabolism in a mouse model of endometriosis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1042826 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26880940_1.fastq.gz | Fastqsanger.gz | |||
| SRR26880940_2.fastq.gz | Fastqsanger.gz | |||
| SRR26880941_1.fastq.gz | Fastqsanger.gz | |||
| SRR26880941_2.fastq.gz | Fastqsanger.gz | |||
| SRR26880942_1.fastq.gz | Fastqsanger.gz |
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Project description:Microbiome dysregulation affects the estrogen metabolism (estrobolome) profile which in turns affects the immunological response. Estrogen hormone is an essential hormone that regulates the sexual activity in females as well as immune response in both sexes. Endometriosis is one of complicated disorder influnce the fertility of females due to escape of endometrial tissue into peritoneal cavity where the immunotoxicity will be undertaken. This study designed to investigate if there is any correlation between the microbiome dyregulation with the severity of endometriosis outcomes.
2023-12-08 | GSE248213 | GEO
Project description:IntroductionEndometriosis is a painful disease that affects around 5% of women of reproductive age. In endometriosis, ectopic endometrial cells or seeded endometrial debris grow in abnormal locations including the peritoneal cavity. Common manifestations of endometriosis include dyspareunia, dysmenorrhea, chronic pelvic pain and often infertility and symptomatic relief or surgical removal are mainstays of treatment. Endometriosis both promotes and responds to estrogen imbalance, leading to intestinal bacterial estrobolome dysregulation and a subsequent induction of inflammation.MethodsIn the current study, we investigated the linkage between gut dysbiosis and immune metabolic response in endometriotic mice. Ovariectomized BALB/c mice received intraperitoneal transplantation of endometrial tissue from OVX donors (OVX+END). Control groups included naïve mice (Naïve), naïve mice that received endometrial transplants (Naive+END) and OVX mice that received the vehicle (OVX+VEH). Colonic content was collected 2 weeks post-transplantation for 16s rRNA pyrosequencing and peritoneal fluid was collected to determine the phenotype of inflammatory cells by flow cytometry.ResultsWe noted a significant increase in the number of peritoneal fluid cells, specifically, T cells, natural killer (NK) cells, and NKT cells in OVX+END mice. Phylogenetic taxonomy analysis showed significant dysbiosis in OVX+END mice, with an increase in abundance of Phylum Tenericutes, Class Mollicutes, Order Aneroplasmatales, and Genus Aneroplasma, and a decrease in Order Clostridiales, and Genus Dehalobacterium, when compared to OVX+VEH controls. The metabolomic profile showed an increase in some tricarboxylic acid cycle (TCA)-related metabolites accompanied by a reduction in short-chain fatty acids (SCFA) such as butyric acid in OVX+END mice. Additionally, the mitochondrial and ATP production of immune cells was enforced to a maximal rate in OVX+END mice when compared to OVX+VEH mice.ConclusionThe current study demonstrates that endometriosis alters the gut microbiota and associated immune metabolism.
| S-EPMC10748389 | biostudies-literature
Project description:Mechanisms of immune dysregulation against established tumors are relatively well understood. Much less is known about the role of immune effectors against cancer precursor lesions. Endometrioid and clear cell ovarian tumors may partly derive from endometriosis, a commonly diagnosed chronic inflammatory disease. We performed here the most comprehensive immune gene expression analysis of pelvic inflammation in endometriosis and endometriosis-associated ovarian cancer (EAOC). RNA was extracted from 120 paraffin tissue blocks comprising of normal endometrium (n=32), benign endometriosis (n=30), atypical endometriosis (n=15) and EAOC (n=43). Serous tumors (n=15) were included as non-endometriosis associated controls. The immune microenvironment was profiled using Nanostring and the nCounter® GX Human Immunology Kit, comprising probes for a total of 511 immune genes. Please note that 3 normal endometrium samples did not pass the array quality filtering and therefore excluded in the data analyses.
2015-01-07 | E-GEOD-57545 | biostudies-arrayexpress
Project description:Mechanisms of immune dysregulation against established tumors are relatively well understood. Much less is known about the role of immune effectors against cancer precursor lesions. Endometrioid and clear cell ovarian tumors may partly derive from endometriosis, a commonly diagnosed chronic inflammatory disease. We performed here the most comprehensive immune gene expression analysis of pelvic inflammation in endometriosis and endometriosis-associated ovarian cancer (EAOC).
2015-01-07 | GSE57545 | GEO
Project description:We performed gene expression analysis human peritoneal endometriosis lesions, eutopic endometrium from endometriosis patients and peritoneum form endometriosis patients.The goal of the study was to analyse gene expression differences between peritoneal endometriosis lesion and eutopic endometrium and peritoneal endometriosis lesion and peritoneum.
2012-12-06 | E-MTAB-694 | biostudies-arrayexpress
Project description:Endometriosis is a benign gynecological condition that causes significant morbidity due to reduced fertility, pelvic pain and inflammatory dysfunctions. High-fat dietary intake has been linked to higher systemic inflammation and oxidative stress, which are both features of women with endometriosis. We evaluated the effects of high-fat diet (HFD) on endometriosis progression using immunocompetent mouse model wherein ectopic lesion was induced in wildtype and kruppel-like factor 9 (KLF9)- null donor mice. Results showed that HFD leads to increased ectopic lesion numbers and higher body weight gain. The HFD-promotion of lesion establishment was associated with decreased stromal estrogen receptor 1 and progesterone receptor expression, increased macrophage infiltration, and enhanced expression of pro-inflammarory and pro-oxidative stress pathway genes. Further, lesion-bearing mice had higher peritoneal fluid TNF-α and elevated local/systemic redox status than control-fed mice.
2017-04-23 | GSE80603 | GEO
Project description:Retrograde menstruation is considered a major reason for the development of endometriosis. The syngeneic transplantation mouse model is an endometriosis animal model that is considered to mimic retrograde menstruation. However, it remains poorly understood which genetic signatures of endometriosis are reflected in this model. Here, we employed an in vivo syngeneic mouse endometriosis model and identified differentially expressed genes (DEGs) between the ectopic and eutopic tissues using microarray analysis.
2022-02-28 | GSE190209 | GEO
Project description:Endometriosis, an estrogen-dependent, progesterone-resistant, inflammatory disorder affects 10% of reproductive-age women. It is diagnosed and staged at surgery, resulting in an 11-year latency from symptom onset to diagnosis, underscoring the need for less invasive, less expensive approaches. Since the uterine lining (endometrium) in women with endometriosis has altered molecular profiles, we tested whether molecular classification of this tissue can distinguish and stage disease. We developed classifiers using genomic data from n=148 archived endometrial samples from women with endometriosis or without endometriosis (normal controls or with other common uterine/pelvic pathologies) across the menstrual cycle and evaluated their performance on independent sample sets. Classifiers were trained separately on samples in specific hormonal milieu, using margin tree classification, and accuracies were scored on independent validation samples. Classification of samples from women with endometriosis or no endometriosis involved two binary decisions each based on expression of specific genes. These first distinguished presence or absence of uterine/pelvic pathology and then no endometriosis from endometriosis, with the latter further classified according to severity (minimal/mild or moderate/severe). Best performing classifiers identified endometriosis with 90-100% accuracy, were cycle phase-specific or independent, and utilized relatively few genes to determine disease and severity. Differential gene expression and pathway analyses revealed immune activation, altered steroid and thyroid hormone signaling/metabolism and growth factor signaling in endometrium of women with endometriosis. Similar findings were observed with other disorders versus controls. Thus, classifier analysis of genomic data from endometrium can detect and stage pelvic endometriosis with high accuracy, dependent or independent of hormonal milieu. We propose that limited classifier candidate-genes are of high value in developing diagnostics and identifying therapeutic targets. Discovery of endometrial molecular differences in the presence of endometriosis and other uterine/pelvic pathologies raises the broader biological question of their impact on the steroid hormone response and normal functions of this tissue. We analyzed endometrial samples from n=148 women without or with endometriosis and/or other uterine/pelvic pathologies, using whole genome microarrays.
2014-10-01 | E-GEOD-51981 | biostudies-arrayexpress
Project description:Nude mouse model of endometriosis
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Project description:Ageing and age-related brain disorders are typically concomitant with cellular mitochondrial dysfunction and metabolic dysregulation in immune cells. However, whether and how immunometabolic dysregulation in the brain affects neurological function are incompletely understood. Here we reveal the presence of metabolic dysregulation within microglia, the brain-resident immune cells, in aged mice. We discover that microglia with dysregulated immunometabolism, induced by dysfunctional mitochondria, initially act as triggers of brain ageing-related neurological dysfunctions in mice, which are mechanistically driven by microglial immunometabolic disturbance-induced inflammaging response depending on neuroimmune cGAS-STING pathway. We present evidence that a combined treatment targeting both metabolism and neuroinflammation partially rescues brain ageing in mice. These findings establish a causal link between immunometabolism, neuroimmunity, and brain ageing, underscoring the significance of tightly regulated immunometabolism in age-associated neurological diseases.
2025-04-28 | GSE266053 | GEO