Maternal gut microbial legacy shapes intestinal health and colitis susceptibility of offspring
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE298759 | GEO | 2026/02/18
REPOSITORIES: GEO
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Project description:Maternal gut microbial legacy shapes intestinal health and colitis susceptibility of offspring
| PRJNA1271060 | ENA
Project description:The goal of this study was to understand the link between maternal oral dysbiosis and the gut health of offspring. We demonstrate that maternal oral dysbiosis can have lasting health impacts on offspring. Ligature-induced periodontitis in mothers promotes the expansion of oral pathobionts in the mouth, which are transmitted to the infant gut, rendering offspring more susceptible to enteritis. Notably, although these maternal oral pathobionts are eradicated as the microbiota matures, the imprinted susceptibility to enteritis persists into adulthood.
2025-06-13 | GSE297306 | GEO
Project description:The intestinal microbiome forms dynamic ecosystem whose balanced composition and functioning are essential for maintaining overall gut health and well-being in living organisms. In broilers, dysbiosis disrupts the microbiota-host balance, often without obvious clinical symptoms but with intestinal inflammation, leading to impaired animal performance and significant economic losses. This study utilizes an in vivo model of dysbiosis to investigate the blood proteome response of broilers to intestinal imbalance. Microscopic histological changes in the gut (shorter villi, increased crypt depth, p<0.0001) were observed in the duodenal and jejunal tissue of challenged birds. Elevated levels of permeability markers faecal ovotransferrin (p < 0.0001) and serum iohexol (p= 0.0009) additionally indicated increased intestinal permeability in challenged group compared to control. The MS/MS-based proteomics analysis was performed on broilers’ blood plasma enabling identification of 388 proteins, 25 of which demonstrated significant difference between the groups. Functional analysis showed activation of immune response, signalling, and interspecies interaction, while proteins related to cellular physiology, cell-cell communication, and extracellular matrix (ECM) processes were suppressed. Protein-protein interaction (PPI) analysis revealed two clusters of downregulated proteins involved in ECM organization and cell adhesion. These results suggest that the dysbiosis challenge alters plasma protein expression as the host prioritizes immune defense over structural maintenance. The activation of immune processes and suppression of ECM pathways highlight potential biomarkers and therapeutic targets for addressing dysbiosis.
2025-07-14 | PXD056546 | Pride
Project description:Intrauterine exposure to disturbed maternal glucose metabolism is associated with adverse consequences for the offspring. Hepatic disorders in affected offspring emerge in early development; thus, detection of disease biomarkers at an early stage may elucidate the underlying mechanisms of maternal hyperglycemia-induced metabolic disease and improve timely diagnosis and treatment strategies. To systematically study the molecular consequences of maternal hyperglycemia, we used data independent acquisition (DIA) proteomics and compared the molecular profiles of liver of three days old wild-type piglets born to a transgenic hyperglycemic pig model with those of wild-type piglets born to normoglycemic mothers.
2023-07-10 | PXD040305 | Pride
Project description:Aside from the perinatal complications associated with low birth weight, individuals born with intra-uterine growth restriction suffer from chronic diseases late in life that ultimately lead to a shortened lifespan. These late life metabolic sequelae of low birth weight include obesity and metabolic syndrome, diabetes mellitus, cardiovascular disease, hypertension, stroke, dyslipidemia, and non-alcoholic fatty liver disease/steatohepatitis. Animal models employing perinatal calorie restriction recapitulate the observations made in humans. Interestingly, if continued calorie restriction is employed post-natally the late life sequelae of intra-uterine growth restriction are ameliorated. These observations linking both fetal and early post natal growth to later health is now termed the developmental origins of health and disease. To further our understanding of the mechanism of how early growth affects late life health we have employed Affymetrix microarray-based expression profiling to characterize hepatic gene expression in a rat model of maternal semi-nutrient restriction. In these experiments we have limited maternal calorie intake to 50% of normal so as to create 3 groups of animals: Control (Con) male offspring born to mothers who were fed normally throughout gestation and lactation; intra-uterine calorie restricted male offspring (IUCR) born to mothers who had 50% restriction of calories from e11 to e21; and combined intra-uterine and post-natal calorie restriction (IPCR) male offspring who were born to mothers who received calorie restriction during both fetal growth (e11 to e21) and post-natally (p1-p21). Livers were collected at p21(day 21 of life) for Con and IPCR groups (IUCR withheld owing to ‘catch up” growth), and at p450 (day 450 of life) for Con, IUCR, and IPCR. The profiling data reveals clear alteration of circadian cycling at P21, and subtle changes for circadian gene expression at p450. In addition, a clear transcriptional response is found during active calorie restriction at p21 but an absence of a transcriptional response late in life at p450. Transcritional studies have been performed using Affymetrix Rat Gene 1.0 arrays for the following treatment groups, with each group run in triplicate (each replicate from separate littermates): Day 21 Control, Day 21 IPCR, Day 450 Con, Day 450 IUCR, Day 450 IPCR
2014-06-01 | E-GEOD-41709 | biostudies-arrayexpress
Project description:We used microarrays to compare the gene expression profile in cultured primary neurospheres derived from the subventricular zone of adult (2 m.o.) offspring of mothers treated with PBS or methylglyoxal during pregnancy Primary neurospheres derived from 2-month-old adult CD1 mice born to mothers treated with PBS or MG twice daily from gestational day 12 until delivery were collected, and total RNA extracted. cDNA was hybridized on Affymetrix Mouse Gene 2.0 ST Array and gene expression was analyzed using Partek software. In total, 3 PBS treated and 3 MG treated mice were used.
2016-03-31 | E-GEOD-79737 | biostudies-arrayexpress
Project description:Aside from the perinatal complications associated with low birth weight, individuals born with intra-uterine growth restriction suffer from chronic diseases late in life that ultimately lead to a shortened lifespan. These late life metabolic sequelae of low birth weight include obesity and metabolic syndrome, diabetes mellitus, cardiovascular disease, hypertension, stroke, dyslipidemia, and non-alcoholic fatty liver disease/steatohepatitis. Animal models employing perinatal calorie restriction recapitulate the observations made in humans. Interestingly, if continued calorie restriction is employed post-natally the late life sequelae of intra-uterine growth restriction are ameliorated. These observations linking both fetal and early post natal growth to later health is now termed the developmental origins of health and disease. To further our understanding of the mechanism of how early growth affects late life health we have employed Affymetrix microarray-based expression profiling to characterize hepatic gene expression in a rat model of maternal semi-nutrient restriction. In these experiments we have limited maternal calorie intake to 50% of normal so as to create 3 groups of animals: Control (Con) male offspring born to mothers who were fed normally throughout gestation and lactation; intra-uterine calorie restricted male offspring (IUCR) born to mothers who had 50% restriction of calories from e11 to e21; and combined intra-uterine and post-natal calorie restriction (IPCR) male offspring who were born to mothers who received calorie restriction during both fetal growth (e11 to e21) and post-natally (p1-p21). Livers were collected at p21(day 21 of life) for Con and IPCR groups (IUCR withheld owing to ‘catch up” growth), and at p450 (day 450 of life) for Con, IUCR, and IPCR. The profiling data reveals clear alteration of circadian cycling at P21, and subtle changes for circadian gene expression at p450. In addition, a clear transcriptional response is found during active calorie restriction at p21 but an absence of a transcriptional response late in life at p450.
2014-06-01 | GSE41709 | GEO
Project description:The aim of this study was to investigate the causative effect of CS induced dysbiosis on obesity and insulin resistance in a high-fat diet induced obese (DIO) mouse model. Male germ-free BALB/c mice were humanized by fecal microbiota transfer using samples from children born by CS or VD and fed HFD for 16 weeks. Adipose tissue was sampled for RNAseq at study termination.
2024-08-01 | GSE254801 | GEO
Project description:Maternal obesity programs the offspring to cardiovascular disease, insulin resistance, and obesity. We sequenced and profiled the cardiac miRNAs that were dysregulated in the hearts of baboon fetuses born to a high fat / high fructose diet fed mothers compared to a regular diet fed mothers. Fetal hearts were collected from baboon fetuses born to obese and lean mothers, total RNA was isolated, and fetal cardiac miRNA were sequenced and profiled
2013-02-01 | E-GEOD-43323 | biostudies-arrayexpress
Project description:Modern lifestyle is associated with a major consumption of ultra-processed foods (UPF) due to their practicality and palatability. The ingestion of emulsifiers, a main additive in UPFs, has been related to gut inflammation, microbiota dysbiosis, adiposity and obesity. Maternal unbalanced nutritional habits during embryonic and perinatal stages perturb offspring’s long-term metabolic health, thus increasing obesity and associated comorbidity risk. However, whether maternal emulsifier consumption influences developmental programming in the offspring remains unknown. Here we show that, in mice, maternal consumption of dietary emulsifiers (1% CMC and 1% P80 in drinking water), during gestation and lactation, perturbs the development of hypothalamic energy balance regulation centers of the progeny, leads to metabolic impairments, cognition deficits and induces anxiety-like traits in a sex-specific manner. Our findings support the notion that maternal consumption of emulsifiers, common additives of UPFs, causes mild metabolic and neuropsychological malprogramming in the progeny. Our data call for nutritional advice during gestation.
2023-07-31 | GSE231769 | GEO