Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1057604 | ENA |
REPOSITORIES: ENA
Similar Datasets
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: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:We performed single-cell RNA sequencing (scRNA-seq) using the 10x Genomics platform to characterize pancreatic immune cell populations in germ-free (GF) and specific-pathogen-free (SPF) mice with cerulein-induced acute pancreatitis (AP). scRNA-seq analysis identified distinct neutrophil subpopulations influenced by gut microbiota presence. SPF mice showed enrichment of pro-inflammatory neutrophil clusters associated with increased neutrophil extracellular trap (NET) formation, whereas GF mice exhibited neutrophil subsets expressing reparative and protective signatures. Our data highlight the role of gut microbiota in shaping immune responses during AP.
2025-08-20 | GSE301305 | 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 |