Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1057604 | ENA |
REPOSITORIES: ENA
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Project description:Microplastics represent a growing environmental concern for the oceans due to their potential capability to adsorb different classes of pollutants, thus representing a still unexplored source of exposure for aquatic organisms. In this study polystyrene (PS) microplastics were characterized for their capability to adsorb pyrene (PYR) as model compound for polycyclic aromatic hydrocarbons, and transfer this chemical to filter feeding mussels Mytilus galloprovincialis. Gene expression analyses of Mytilus galloprovincialis exposed to polystyrene (PS) microplastics and to polystyrene contaminated with pyrene (PS-PYR) have been performed trough a DNA microarray platform.
2014-12-27 | GSE57460 | GEO
Project description:Microplastics (MPs) as widespread contamination pose high risk for aquatic organisms.Intestinal microbiotahas have high interaction with immune system of host body. In this study, intestinal microbiota of zebrafish after Polystyrene (PS-MPs) exposure were characterized by 16S rDNA amplicon sequencing. We found that 100nm and 200μm PS-MPs exposure significantly increased diversity of intestinal microbiota and all the three sizes of PS-MPs increased abundance of pathogenic bacteria.
2019-10-01 | GSE136108 | GEO
Project description:Background: Acute pancreatitis (AP) is a common severe digestive disorder, with severity linked to high-fat diets (HFD). HFD may exacerbate AP by promoting inflammation and altering gut microbiota. Astragalus polysaccharides (APS) possess anti-inflammatory properties, but it is unclear if APS supplementation can mitigate HFD's detrimental effects on AP by modulating gut microbiota. This study investigates the mechanisms by which APS improves HFD-induced AP exacerbation. In this study, C57BL/6 mice were fed HFD or a standard diet, with or without APS, for 12 weeks. AP was induced via intraperitoneal caerulein injection. Analyses included ELISA, Western blotting, histology, immunohistochemistry, immunofluorescence, single-cell RNA sequencing (scRNA-seq), 16S rRNA sequencing of gut microbiota, and short-chain fatty acid (SCFA) analysis to evaluate inflammation and cellular changes. Results: HFD significantly increased AP severity, indicated by elevated serum enzyme and pro-inflammatory cytokine levels, along with extensive pancreatic damage. Single-cell RNA sequencing (scRNA-seq) showed a notable rise in ICAM1+ neutrophils and activation of the NF-κB/necroptosis pathway in HAP mice. APS alleviated these effects by decreasing ICAM1+ neutrophil infiltration, downregulating the NF-κB pathway, and reducing necroptosis. Moreover, APS restored gut microbiota balance, significantly boosting Lactobacillus reuteri (L. reuteri) abundance and propionate (PA) levels. Treatments with L. reuteri and PA independently mitigated HFD-induced AP severity, indicating that APS's protective effects are microbiota-dependent. Conclusion: APS improves HFD-induced gut dysbiosis and intestinal barrier dysfunction by enriching L. reuteri and PA, effectively reducing AP exacerbation. Our findings highlight the gut-pancreas axis as a promising target for addressing AP severity.
2024-10-22 | GSE279876 | GEO
Project description:Acetaminophen is a widely used antipyretic and analgesic drug, and its overdose is the leading cause of drug-induced acute liver failure. This study aimed to investigate the effect and mechanism of Lacticaseibacillus casei Shirota (LcS), an extensively used and highly studied probiotic, on acetaminophen-induced acute liver injury. C57BL/6 mice were gavaged with LcS suspension or saline once daily for 7 days before the acute liver injury was induced via intraperitoneal injection of 300 mg/kg acetaminophen. The results showed that LcS significantly decreased acetaminophen-induced liver and ileum injury, as demonstrated by reductions in the increases in aspartate aminotransferase, total bile acids, total bilirubin, indirect bilirubin and hepatic cell necrosis. Moreover, LcS alleviated the acetaminophen-induced intestinal mucosal permeability, elevation in serum IL-1α and lipopolysaccharide, and decreased levels of serum eosinophil chemokine (eotaxin) and hepatic glutathione levels. Furthermore, analysis of the gut microbiota and metabolome showed that LcS reduced the acetaminophen-enriched levels of Cyanobacteria, Oxyphotobacteria, long-chain fatty acids, cholesterol and sugars in the gut. Additionally, the transcriptome and proteomics showed that LcS mitigated the downregulation of metabolism and immune pathways as well as glutathione formation during acetaminophen-induced acute liver injury. This is the first study showing that pretreatment with LcS alleviates acetaminophen-enriched acute liver injury, and it provides a reference for the application of LcS.
2023-07-26 | PXD044099 |
Project description:Despite recent advances, severe acute pancreatitis (SAP) remains an extremely lethal inflammation with limited treatment options. Here, we provide compelling evidence of GV-971 (sodium oligomannate), an anti-Alzheimer's medication, as being a protective agent in various mouse SAP models. Microbiome sequencing, along with fecal microbiota transplantation and mass cytometry technology, unveiled that GV-971 reshapes the gut microbiota, increasing Faecalibacterium populations and modulating both peripheral and intestinal immune systems. A metabolomics analysis of cecal contents from GV-971–treated SAP mice further identified short-chain fatty acids, including propionate and butyrate, as key metabolites in inhibiting macrophage M1 polarization and subsequent lethal inflammation by blocking the MAPK pathway. These findings suggest GV-971 as a promising therapeutic for SAP by targeting the microbiota metabolic immune axis.
2024-07-04 | GSE271034 | GEO
Project description:Gut microbiota plays an important role during early development via bidirectional gut- brain signaling. We aimed to explore the potential link between gut microbiota/gut derived metabolites and sympathoadrenal stress responsivity
2018-11-25 | GSE122754 | GEO
Project description:Microplastics (MPs) are considered as one of the main reasons for male and female infertility. However, the reproductive toxicity and its related mechanisms are understood by animal models with acute exposure to MPs at present. In the study, we show the low-dose polystyrene microplastics (PSMPs) exposure results in severely abnormal reproduction in female, but not male in mouse model, exhibiting failed oocyte meiotic maturation. Mechanistically, the PSMPs exposure induces the over-activation of cell metabolism pathways, insufficient HDACs and H4K16 hyperacetylation in oocytes in vivo and in vitro. By addition of HDAC3 inhibitor, the failed oocyte maturation, over-activation of cell metabolism pathways and H4K16 hyperacetylation are recapitulated, and the overexpression of HDAC3 can rescue the defects of meiotic maturation induced by PSMPs. Our observations suggest a direct link of the maturation defects induced by PSMPs to HDAC3 insufficiency. Thus, we propose the potential treatments for therapy of the failed meiotic maturation of oocyte from women highly exposed to MPs by activating or supplying HDAC3.
2024-03-06 | GSE259264 | GEO