Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1061839 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27455439.fastq.gz | Fastqsanger.gz | |||
| SRR27455440.fastq.gz | Fastqsanger.gz | |||
| SRR27455441.fastq.gz | Fastqsanger.gz | |||
| SRR27455442.fastq.gz | Fastqsanger.gz | |||
| SRR27455443.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 32 |
Similar Datasets
Project description:Markus W. Covert, Thomas H. Leung, Jahlionais E. Gaston & David Baltimore. Achieving stability of lipopolysaccharide-induced NF-kappaB activation. Science 309, 5742 (2005).
Preterm birth is the single biggest cause of significant neonatal morbidity and mortality, and the incidence is rising. Development of new therapies to treat and prevent preterm labour is seriously hampered by incomplete understanding of the molecular mechanisms that initiate labour at term and preterm. Computational modelling provides a new opportunity to improve this understanding. It is a useful tool in (i) identifying gaps in knowledge and informing future research, and (ii) providing the basis for an in silico model of parturition in which novel drugs to prevent or treat preterm labour can be "tested". Despite their merits, computational models are rarely used to study the molecular events initiating labour. Here, we present the first attempt to generate a dynamic kinetic model that has relevance to the molecular mechanisms of preterm labour. Using published data, we model an important candidate signalling pathway in infection-induced preterm labour: that of lipopolysaccharide (LPS) -induced activation of Nuclear Factor kappa B. This is the first model of this pathway to explicitly include molecular interactions upstream of Nuclear Factor kappa B activation. We produced a formalised graphical depiction of the pathway and built a kinetic model based on ordinary differential equations. The kinetic model accurately reproduced published in vitro time course plots of Lipopolysaccharide-induced Nuclear Factor kappa B activation in mouse embryo fibroblasts. In this preliminary work we have provided proof of concept that it is possible to build computational models of signalling pathways that are relevant to the regulation of labour, and suggest that models that are validated with wet-lab experiments have the potential to greatly benefit the field.
2024-09-02 | BIOMD0000000489 | BioModels
Project description:LPS response during systemic infection
| PRJNA378232 | ENA
Project description:Placental insufficiency is implicated in the intrauterine infection-associated spontaneous preterm birth. Using a mouse model of LPS-induced intrauterine inflammation that leads to preterm delivery, RNA-seq study was performed in the placenta at gestational day 17 to assess the transcriptome changes.
2020-11-27 | GSE151728 | GEO
Project description:Background: Neonatal infection and sepsis are common for preterm infants due to their immature immune system. Early diagnosis is important for effective treatment but few early markers of systemic and neuro-inflammatory responses in neonates are known. We hypothesized that systemic infection with Gram-positive Staphylococcus epidermidis (SE) induces acute changes to proteins in plasma and cerebrospinal fluid (CSF), potentially affecting the immature brain of preterm neonates. Methods: Using preterm pigs as model for preterm infants, plasma and CSF samples were collected up to 24 h after SE infection and investigated by untargeted mass spectrometry (MS)-based proteomics. Selected differential proteins were further studied in vitro assays. Results: The clinical signs of sepsis and neuroinflammation in SE-infected piglets were associated with changes in multiple CSF and plasma proteins. Eight plasma proteins, including APOA4, haptoglobin, MBL1, vWF, LBP and sCD14, were affected already 6 h after infection. Likewise, acute phase reactants, including complement components, showed a time-dependent activation pattern after infection. Feeding bovine colostrum reduced the sepsis-related change in clinical parameters as well as plasma proteins. Neuroinflammation-related neuropeptide Y (NPY), IL-18 and MMP-14 showed distinct changes in the CSF and several brain regions (prefrontal cortex, PVWM, hippocampus) 24 h after infection. These changes were verified in TLR2 agonist-challenged primary microglia cells, where exogenous NPY suppressed the inflammatory response. Conclusion: Systemic infection with Gram-positive SE induces inflammation with rapid proteome changes in plasma and CSF in preterm newborn pigs. The observed early markers of sepsis and neuroinflammation in preterm pigs may serve as novel biomarkers for sepsis in preterm infants.
2020-05-26 | PXD016013 | Pride
Project description:LPS response during systemic Chlamydia infection
| PRJNA378227 | ENA
Project description:Background: Preterm infants are at high risk of infection and sepsis, which is associated with arginine (ARG) deficiency. Optimal nutrition for preterm newborns suspected with infection is critical to prevent sepsis development. Citrulline (CIT) supplementation is known to prevent sepsis in adult rodents, by maintaining sufficient blood ARG levels and vascular stabilization. We hypothesized that CIT therapy improve sepsis outcomes in infected preterm newborns via CIT and ARG metabolism.Results: After infection, oral CIT supplementation led to higher mortality, blood bacterial load, and circulating and hepatic inflammation, compared with the infected controls. Intravenous CIT administration also showed increased inflammation and bacterial burdens without increased mortality. Liver transcriptomics and data from in vitro blood stimulation indicated that CIT induces enhanced immunosuppression, which may impair resistance response to bacteria at early stage of infection and later cause excessive inflammation and tissue damage. Conclusion: Early stage of CIT supplementation exacerbates sepsis severity in infected preterm pigs, likely via induced enhanced systemic immunosuppression.
2023-11-20 | GSE247865 | GEO
Project description:<p>Preterm birth (PTB, born before 37 weeks of gestation) is a leading cause of neonatal mortality and post-natal morbidity. PTB affects one in nine all live births in the U.S. Notably, the highest rate of PTB occurs among African Americans (one in six). PTB is a complex trait, likely determined by multiple environmental and genetic factors and their interactions. We demonstrated strong familial aggregation of preterm and low birthweight in the US Blacks and Whites (Wang et al, NEJM, <a href="http://www.ncbi.nlm.nih.gov/pubmed/7491139">1995</a>) and conducted the largest candidate gene study of preterm birth at that time (Hao et al, HMG, <a href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=DetailsSearch&term=14976157">2004</a>). We showed that a subset of mothers with certain metabolic gene variants are particularly vulnerable to the adverse effects of cigarette smoking on low birthweight and preterm births (Wang et al, JAMA, <a href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=DetailsSearch&term=11779261">2002</a>). We also published a number of papers that examined the effect of maternal pre-pregnancy BMI, micronutrient status, stress and environmental toxins on the risk of preterm birth and related conditions.</p> <p>This project, supported by a grant from the NICHD (2R01HD41702, PI, Xiaobin Wang), aimed to conduct a genome-wide association study (GWAS) and apply advanced statistical methods to identify susceptibility loci of PTB in a predominantly urban low-income African American sample, a subset of the Boston Birth Cohort.</p> <p>PUBLIC HEALTH REVELANCE: We anticipate that this study will lead to the identification of novel genetic loci of PTB and gene-environment interactions. Such findings not only will provide important insights into mechanisms leading to PTB, but also may help identify women at high-risk of PTB, which in turn, may lead to the development of early and targeted interventions that can prevent PTB or mitigate the severity and consequences of PTB.</p>
| phs000332 | dbGaP
Project description:The inflammatory mediator IL6 induced by LPS, which signals via TLR4, has been shown to feedback and augment TLR4 signaling when over-produced in LPS hypersensitive gp130F/F mice. The identity of the LPS/TLR4 responsive inflammatory signaling pathways and gene networks which are modulated by IL6 are unknown. Therefore, to understand the molecular consequences of gp130 hyperactivity in non-haemopoietic tissue on LPS-induced systemic inflammation, global gene expression profiling of livers was performed.
2011-05-17 | GSE29311 | GEO
Project description:Purpose: No gene expression profiles for the placenta in LPS-induced preterm labor mouse model have been published. The goal of this study was to obtain a comprehensive catalog of differentially expressed genes (DEGs) in the placenta using RNA-seq. Methods: Preterm labor mouse model (P) and control pregnancy group (C) were gained using a protocol from R. Migale, et al., BMC MED 14 (2016):86. Briefly, on day 15.5 of gestation, an abdominal minilaparotomy was performed. The upper right uterine horn between the first and second sacs received injections of saline (C) or 20 mg E. coli LPS serotype O55:B5 (Sigma-Aldrich, Gillingham, UK) (P) to model preterm labor. Six hours after injections of LPS, the mice were sacrificed and placentas were excised and immediately snap-frozen in liquid nitrogen before being stored at −80°C for subsequent analysis. Placental mRNA profiles were generated by deep sequencing using Illumina seq 2500. The sequence reads that passed quality filters were analyzed at the transcript isoform level with TopHat followed by Cufflinks. qRT–PCR validation was performed using TaqMan and SYBR Green assays. Results: We mapped about 44 million sequence reads per sample to the mouse genome (build mm8) and 25307 transcripts with TopHat workflow. 155 differentially expressed genes (DEGs) in placenta were identified between the preterm group and control group, with a fold change ≥1.5 and p value <0.05. 61 inflammation-related genes occupied the dominant role. 7 of these were validated with qRT–PCR. Conclusions: Our study represents the first detailed analysis of transcriptomes in placenta in LPS-induced preterm labor mouse model by RNA-seq technology. Dominant inflammatory profile in this model was gained, which gives us a better understanding of the exact molecular processes involved in the development of preterm labor after infection.
2018-05-26 | GSE114939 | GEO
Project description:LPS-induced systemic inflammation mediates a protective action on ischemic injury via microglia. We used RNA sequencing analysis (RNA-seq) to gain molecular insights into microglia-mediated protection of cerebral infarction.
2023-12-19 | GSE244358 | GEO