Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1162656 | ENA |
REPOSITORIES: ENA
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Project description:Subclinical necrotic enteritis (SNE) is one of the serious threats to the poultry industry. Probiotics have been proven to exert the beneficial effects in controlling SNE. However, the exact mechanisms of probiotics have not been fully elucidated, and few researchs have focused on their impact on miRNAs. Therefore, the purpose of this study was to explore the miRNA expression profles in the ileum of broiler chickens during probiotic supplement treatment for SNE. 180 newly hatched male chicks were randomly allocated in three groups, including negative control group(NC), SNE infection group(PC) and Bacillus licheniformis H2 pre-treatment group (BL). Illumina high-throughput sequencing was conducted to identify the miRNA expression of three groups. The results showed that 628 miRNAs, including 582 known miRNAs and 46 novel miRNAs, were detected in libraries. The target genes of 57 significantly differentially expressed miRNAs were predicted and annotated, which were found to partly enrich in pathways related to immunity and inflammation such as tumor necrosis factor receptor binding, immune response-regulating signaling pathway, activation of NF-kappaB-inducing kinase activity, interleukin-15 production, Toll-like receptor 2 signaling pathway and MAP kinase tyrosine/serine/threonine phosphatase activity. Our results provided comprehensive miRNA expression profles of these three different treatment groups. And these findings suggested that H2 could exert beneficial effects in controlling SNE may through immune and inflammatory response associated to altered miRNA expression.
2020-06-03 | GSE151627 | GEO
Project description:Acute liver failure (ALF) is a severe consequence of abrupt hepatocyte injury with lethal outcomes. Three toll-like receptor (TLR) agonists, including polyinosinic-polycytidylic acid [poly(I:C)], lipopolysaccharide (LPS), and cytosine-phosphate-guanine oligonucleotide (CpG ODN), respectively, cause severe and acute hepatitis in D-galactosamine (D-GalN) sensitized mice as the experimental ALF animal models. However, the molecular differences in ALF among the three models are unclear. Here, we conducted global proteomic analyses of the three ALF mice models. We identified 227, 321, and 114 differentially regulated proteins and 80,195, and 23 specifically expressed proteins in the poly(I:C)/D-GalN, LPS/D-GalN and CpG ODN/D-GalN groups compared to the control group, respectively. Fifty-two proteins were commonly identified in the three ALF groups. Gene ontology (GO) analyses showed that 45 proteins were located in organelles, 35 proteins were involved in metabolic processes, and 10 proteins were involved in immune system processes. Poly (I:C)- and LPS-specific proteins were mainly distributed in the membrane and endoplasmic reticulum, respectively. LPS-specific proteins were more enriched in metabolic pathways. CpG-specific proteins were mainly related to the ribosome structural composition. In conclusion, our study shows different molecular mechanisms of three TLR agonists in D-GalN induced ALF and provides a useful dataset for the guidance of future studies.
2020-01-19 | PXD017180 |
Project description:Bioinformatic analysis of microarray data was used to identify the regulatory patterns underlying changes in gene expression induced when RAW 264.7 macrophages were stimulated via TLR9 by CpG oligonucleotides (ODN) and/or via TLR3 by poly (I:C). While the genes activated by each ligand mediated similar functions, poly (I:C) elicited a larger and more diverse change in gene expression. Co-stimulation with both ligands accelerated gene expression and synergistically activated genes primarily associated with immune function. This is the first work to compare global changes in gene regulation triggered by distinct TLR pathways and clarify their impact on gene expression.
2009-07-21 | GSE15416 | GEO
Project description:Innate receptors, including Toll like receptors (TLRs), are implicated in pathogenesis of CNS inflammatory diseases such as multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE). TLR response to pathogens or endogenous signals includes production of immunoregulatory mediators. One of these, interferon (IFN)β, a Type I IFN, plays a protective role in MS and EAE. We have previously shown that intrathecal administration of selected TLR ligands induced IFNβ and infiltration of blood-derived myeloid cells into the CNS, and suppressed EAE in mice. We have now extended these studies to evaluate a potential therapeutic role for CNS-endogenous TLR7 and TLR9. Intrathecal application of Imiquimod (TLR7 ligand) or CpG oligonucleotide (TLR9 ligand) into CNS of otherwise unmanipulated mice induced IFNβ expression, with greater magnitude in response to CpG. CNS extraparenchymal CD45+ cells were identified as source of IFNβ. Intrathecal CpG induced infiltration of monocytes, neutrophils, CD4+ T cells and NK cells whereas Imiquimod did not recruit blood-derived CD45+ cells. CpG, but not Imiquimod, had a beneficial effect on EAE, when given at time of disease onset. This therapeutic effect of CpG on EAE was not seen in mice lacking the Type I IFN receptor. In mice with EAE treated with CpG, the proportion of monocytes was significantly increased in the CNS. Infiltrating cells were predominantly localized to spinal cord meninges and demyelination was significantly reduced compared to non-treated mice with EAE. Our findings show that TLR7 and TLR9 signaling induce distinct inflammatory responses in the CNS with different outcome in EAE and point to recruitment of blood-derived cells and IFNβ induction as possible mechanistic links between TLR9 stimulation and amelioration of EAE. The protective role of TLR9 signaling in the CNS may have application in treatment of diseases such as MS.
2021-04-15 | GSE172083 | GEO