Ontology highlight
ABSTRACT:
PROVIDER: PRJNA894691 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22058643_1.fastq.gz | Fastqsanger.gz | |||
| SRR22058643_2.fastq.gz | Fastqsanger.gz | |||
| SRR22058644_1.fastq.gz | Fastqsanger.gz | |||
| SRR22058644_2.fastq.gz | Fastqsanger.gz | |||
| SRR22058645_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 104 |
Similar Datasets
Project description:Air pollution, particularly environmental tobacco smoke, poses significant health risks, especially to pregnant women and their infants. This study explores the difference in response to cigarette smoke (CS) exposure between pregnant and non-pregnant mice by examining lung transcriptomic profiles, neutrophil numbers, key mediators of neutrophil chemotaxis, and gut microbiota composition. Pregnant and non-pregnant mice were exposed to either air or CS. Bronchoalveolar lavage fluid (BALF) was analyzed for inflammatory cells and mediators. RNA sequencing was conducted on lung tissue to identify transcriptomic alterations.
2025-07-21 | GSE302905 | GEO
Project description:Maternal exposure to particulate air pollution increases the incidence and severity of asthma in offspring, yet the mechanisms for this are unclear. Known susceptibility loci are a minor component of this effect. We interrogate a mouse allergic airway disease model to assess epigenetic associations between maternal air pollution exposure and asthma-like responses in offspring. Maternal air pollution exposure increased allergic airway disease severity in adult offspring associated with a suppressed transcriptomic response to allergen. Control progeny showed differential expression of 2842 genes across several important pathways, including the SMAD and TGFβR pathways, whilst air pollutant progeny showed an 80% reduction in differentially expressed genes and abrogation of many pathway associations. Whole genome CpG methylome analysis following allergen challenge detected differential methylation regions across the genome. Approximately 20% of differentially expressed genes were associated with differential methylation. Differentially methylated regions were markedly reduced in offspring of air pollution exposed mothers, and this was most evident in intronic regions and some transposable element classes. This study shows that allergic airways disease in adult offspring of PM2.5 exposed mothers had a markedly repressed transcriptomic response, a proportion of which was associated with identifiable changes in the lung’s methylome. The results point to an epigenetic contribution to the severity of asthma in offspring of mothers exposed to particulate air pollution.
2025-03-12 | GSE285243 | GEO
Project description:Maternal exposure to particulate air pollution increases the incidence and severity of asthma in offspring, yet the mechanisms for this are unclear. Known susceptibility loci are a minor component of this effect. We interrogate a mouse allergic airway disease model to assess epigenetic associations between maternal air pollution exposure and asthma-like responses in offspring. Maternal air pollution exposure increased allergic airway disease severity in adult offspring associated with a suppressed transcriptomic response to allergen. Control progeny showed differential expression of 2842 genes across several important pathways, including the SMAD and TGFβR pathways, whilst air pollutant progeny showed an 80% reduction in differentially expressed genes and abrogation of many pathway associations. Whole genome CpG methylome analysis following allergen challenge detected differential methylation regions across the genome. Approximately 20% of differentially expressed genes were associated with differential methylation. Differentially methylated regions were markedly reduced in offspring of air pollution exposed mothers, and this was most evident in intronic regions and some transposable element classes. This study shows that allergic airways disease in adult offspring of PM2.5 exposed mothers had a markedly repressed transcriptomic response, a proportion of which was associated with identifiable changes in the lung’s methylome. The results point to an epigenetic contribution to the severity of asthma in offspring of mothers exposed to particulate air pollution.
2025-03-12 | GSE285128 | GEO
Project description:There is increasing concern regarding the adverse effects of air pollution on human health, and benzene is a major toxic compound in air pollution. Maternal benzene exposure has been associated with reproductive complications, such as preterm birth, low birth weight, and immunological and neurological complications in the offspring. However, it is poorly understood how benzene induces these complications. Our objective was to establish a full body inhalation mouse model for maternal benzene exposure that mimics clinical phenotypes observed in human populations, and characterize the maternal immune activation and placental response in our model. Here, we report that maternal immune activation triggered by benzene exposure during pregnancy leads to increased resorptions, abnormal placenta development and low birth weight of fetus. More importantly, there is a sexual dimorphic response to benzene exposure in female and male placentas. In the male placenta, the transcriptome changes reveal a more immunologically relevant profile, while females have a metabolically related profile. Furthermore, we discover the sexual dimorphic response could be a consequence of the sexual dimorphism of placenta at baseline, which indicates the significant difference between sexes in terms of the immunological processes in the placenta, both in human and mouse. Therefore, our findings established a benzene exposure mouse model and indicated the sexual dimorphism of placenta, which provides valuable reference for the future pregnancy studies.
2023-07-20 | PXD035085 | Pride
Project description:Introduction: Air pollution is detrimental to a pregnancy with adverse effects in mother and child. It is also known to increase pregnancy complications including risk factors of gestational diabetes. Methods: We investigated the impact of intra-nasal instilled air pollutants upon gestational day 16-19 maternal mouse cardiovascular and metabolic status, placental nutrient transporters, and placental-fetal size and morphology. To further unravel mechanisms, we also examined placental total DNA 5’-hydroxymethylation and bulk RNA sequenced gene expression profiles. Results: Air pollution exposed pregnant mice were tachycardic, hyperglycemic, glucose intolerant and insulin resistant, with no major placental glucose and fatty acid transporter changes, except for a spatial disruption of cells expressing GLUT10 that imports L-dehydroascorbic acid in protecting against oxidative stress. Placentas revealed inflammatory cellular infiltration with associated cellular edema and necrosis, with a paucity of vascularity and hemorrhage. While individual fetal body weights increased, they suffered a reduction in brain cortical thickness. Placental total DNA 5’-hydroxymethylation was 2.5-fold higher, with perturbed gene expression profiles involving key metabolic, inflammatory, transcriptional, cellular polarizing and processing genes and pathways. Discussion: We conclude that gestational exposure to air pollutants incites a maternal inflammatory response resulting in features of maternal gestational diabetes mellitus with altered placental gene expression with associated injury to the placental-fetal unit. Thus, air pollutants adversely impact the health of mother and offspring.
2025-03-07 | GSE261095 | GEO
Project description:The neurotoxicity of air pollution is undefined for sex and APOE alleles. These major risk factors of Alzheimer’s disease (AD) were examined in mice given chronic exposure to nPM, a nano-sized subfraction of urban air pollution. In the cerebral cortex, female mice had two-fold more genes responding to nPM than males. Transcriptomic responses to nPM had sex-APOE interactions in AD-relevant pathways. Only APOE3 mice responded to nPM in genes related to Abeta deposition and clearance (Vav2, Vav3, S1009a). Other responding genes included axonal guidance, inflammation (AMPK, NFKB, APK/JNK signaling), and antioxidant signaling (NRF2, HIF1A). Genes downstream of NFKB and NRF2 responded in opposite directions to nPM. Nrf2 knockdown in microglia augmented NFKB responses to nPM, suggesting a critical role of NRF2 in air pollution neurotoxicity. These findings give a rationale for epidemiologic studies of air pollution to consider sex interactions with APOE alleles and other AD-risk genes.
2020-06-24 | GSE142066 | GEO
Project description:The formation of embryonic muscle fibers during the prenatal period determines the number of muscle fibers after birth. Our previous studies showed that SYISL gene knockout (KO) mice significantly increased the number of total muscle fibers, but the underlying mechanism remains unclear. In this study, we found that the development of embryonic muscle fibers was significantly influenced by the interaction between host SYISL genotype and maternal gut microbiota. SYISL KO alters the composition of the female mice maternal gut microbiota, significantly increases the relative abundance of Prevotella (P<0.05). Fecal microbiota transplantation (FMT) experiments indicated that fecal suspension from KO female mice significantly increased the number of offspring muscle fibers. Our study provides the new evidence for the interaction between maternal single gene and gut microbiota on the embryonic muscle development of the offspring.
2025-02-19 | GSE244822 | GEO
Project description:Maternal secretor status is one of the determinants of human milk oligosaccharides (HMOs) composition, which in turn changes the gut microbiota composition of infants. To understand if this change in gut microbiota impacts immune cell composition, intestinal morphology and gene expression, day 21-old germ-free mice were transplanted with fecal microbiota from infants whose mothers were either secretors (SMM) or non-secretors (NSM) or from infants consuming dairy-based formula (MFM). For each group, one set of mice was supplemented with HMOs. HMO supplementation did not significantly impact the microbiota diversity however, SMM mice had higher abundance of genus Bacteroides, Bifidobacterium, and Blautia, whereas, in the NSM group, there were higher abundance of Akkermansia, Enterocloster, and Klebsiella. In MFM, gut microbiota was represented mainly by Parabacteroides, Ruminococcaceae_unclassified, and Clostrodium_sensu_stricto. In mesenteric lymph node, Foxp3+ T cells and innate lymphoid cells type 2 (ILC2) were increased in MFM mice supplemented with HMOs while in the spleen, they were increased in SMM+HMOs mice. Similarly, serum immunoglobulin A (IgA) was also elevated in MFM+HMOs group. Distinct global gene expression of the gut was observed in each microbiota group, which was enhanced with HMOs supplementation. Overall, our data shows that distinct infant gut microbiota due to maternal secretor status or consumption of dairy-based formula and HMO supplementation impacts immune cell composition, antibody response and intestinal gene expression in a mouse model.
2024-03-12 | GSE260491 | GEO
Project description:We have previously demonstrated that the gut microbiota can play a role in the pathogenesis of conditions associated with exposure to environmental pollutants. It is well accepted that diets high in fermentable fibers such as inulin can beneficially modulate the gut microbiota and lessen the severity of pro-inflammatory diseases. Therefore, we aimed to test the hypothesis that hyperlipidemic mice fed a diet enriched with inulin would be protected from the pro-inflammatory toxic effects of PCB 126.
2020-02-27 | E-MTAB-8798 | biostudies-arrayexpress
Project description:Antibiotics have long-lasting consequences on the gut microbiota with the potential to impact host physiology and health. However, little is known about the transgenerational impact of an antibiotic-perturbed microbiota. Here we demonstrated that adult pregnant female mice inoculated with a gut microbial community shaped by antibiotic exposure passed on their dysbiotic microbiota to their offspring. This dysbiotic microbiota remained distinct from controls for at least 5 months in the offspring without any continued exposure to antibiotics. By using IL-10 deficient mice, which are genetically susceptible to colitis, we showed mice that received an antibiotic-perturbed gut microbiota from their mothers had increased risk of colitis. Taken together, our findings indicate that the consequences of antibiotic exposure affecting the gut microbiota can extend to a second generation.
2017-12-01 | GSE92623 | GEO