Ontology highlight
ABSTRACT:
PROVIDER: PRJNA390780 | ENA |
REPOSITORIES: ENA
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Project description:Inflammation and immunity play a causal role in the pathogenesis of pulmonary vascular remodeling and pulmonary arterial hypertension (PAH). However, the pathways and mechanisms by which inflammation and immunity contribute to pulmonary vascular remodeling remain unknown. RNA sequencing was used to analyze the transcriptome in control and rats injected with monocrotaline (MCT) for 1, 2, 3 and 4 weeks. Using the transcriptional profiling of MCT-induced PAH coupled with bioinformatics analysis, we clustered the differentially expressed genes (DEGs) and chose the increased expression patterns associated with inflammatory and immune response. We found the enrichment of Toll-like receptor (TLR) and NOD-like receptor (NLR) pathways and identified NF-κB-mediated inflammatory and immune profiling in MCT-induced PAH. Pathway-based data integration and visualization showed the dysregulated TLR and NLR pathways, including increased expression of TLR2 and NLRP3, and their downstream molecules. Further analysis revealed that the activation of TLR and NLR pathways was associated with upregulation of damage-associated molecular patterns (DAMPs) and RIPK3-mediated necroptosis was involved in the generation of DAMPs in MCT-induced PAH. Collectively, we identify RIPK3-mediated necroptosis and its triggered TLR and NLR pathways in the progression of pulmonary vascular remodeling, thus, providing novel insights into the mechanisms underlying inflammation and immunity in the pathogenesis of PAH.
2020-05-02 | GSE149713 | GEO
Project description:Human D14+ / CD16+ monocytes were treated with GPBAR1 agonists or controls, and were stimulated with interferon gamma and LPS. At 6 and 24 hours, the cells were profiled by RNAseq
2014-06-10 | GSE57494 | GEO
Project description:Human D14+ / CD16+ monocytes were treated with GPBAR1 agonists or controls, and were stimulated with interferon gamma and LPS. At 6 and 24 hours, the cells were profiled by RNAseq 40 total samples, 5 per group with eight groups. Individual donors used for multiple comparisons, so paired analysis is possible. Control samples include unstimulated cells, and stimulated cells treated with vehicle control (DMSO).
2014-06-10 | E-GEOD-57494 | biostudies-arrayexpress
Project description:Analysis of monocyte-derived dendritic cells (MoDC) gene expression signature induced by TLR agonists the in presence or in the absence of PP2.
2010-06-18 | E-TABM-1018 | biostudies-arrayexpress
Project description:To obtain an insight into host-pathogen interactions in clostridial myonecrosis, we carried out comparative RNA-seq analysis measuring host genes in a murine C. perfringens infection model. Analysis of the murine transcriptome from infected muscle tissues indicated that 270 genes were up-regulated compared to control mock-infected mice. KEGG pathway analysis of these genes revealed an enrichment of Toll-like receptor (TLR) and Nod-like receptor (NLR) signaling components.
2018-03-07 | GSE106657 | GEO
Project description:The reassorted human 2009 pandemic H1N1 (H1N1pdm) virus infected millions of people and caused thousands of deaths with associated immunopathology. Traditional immunosuppressants have limited capabilities in controlling inflammatory responses associated with severe influenza infections. A new therapeutic strategy, therefore, must be developed. We evaluated several adjuvants including toll-like receptor (TLR) agonists, TLR independent adjuvants and Complete Freund’s adjuvant (CFA) for limiting severe H1N1pdm infection outcomes in a mouse model. In contrast to the TLR agonists and TLR independent adjuvants, CFA which contains multiple pattern recognition receptor (PRR) agonists significantly restrained pro-inflammatory responses and promoted survival in mice from lethal H1N1pdm infection. CFA reduced expression of the plamacytoid dendritic cell (pDC) markers and interferon alpha (IFN-α) after infection, whereas it elevated the T regulatory (Treg) cell suppressive molecules galectin-1 and CTLA-4 expression. Consequently, Th1 cell differentiation and CD8+ effector T cell responses were diminished via downregulated myeloid DC (mDC) costimulation. Furthermore, CTLA-4 expressing Treg cells were dramatically increased when the CFA primed splenocytes were restimulated with its stimuli-killed mycobacterium tuberculosis (M. TB). The elevated CTLA-4 on Treg cells led to reduced CD86 expressing pDCs/mDCs and less CD4+ effector T cells. Overall, our study highlights that the stimuli of innate immunity potentially controls overactive host immune responses in certain situations, and the uncovered mechanism(s) sheds light on the development of anti-influenza therapies. C57B6/J Mice were treated with CFA at day -2 and day 2 post H1N1pdm infection. Weight loss and lethality were monitored post infection. At day 3 and day 5 lung tissues were collected for RNA extraction and expression array analysis.
2014-09-10 | E-GEOD-41088 | biostudies-arrayexpress
Project description:Myeloid lineage cells use TLRs to recognize and respond to diverse microbial ligands. Although unique transcription factors dictate the outcome of specific TLR signaling, whether lineage-specific differences exist to further modulate the quality of TLR-induced inflammation remains unclear. Comprehensive analysis of global gene transcription in human monocytes, monocyte-derived macrophages and monocyte-derived dendritic cells stimulated with various TLR ligands identifies multiple lineage-specific, TLR-responsive gene programs. Monocytes are hyperresponsive to TLR7/8 stimulation that correlates with higher expression of the receptors. While macrophages and monocytes express similar levels of TLR4, macrophages, but not monocytes, upregulate Interferon-Stimulated Genes (ISGs) in response to TLR4 stimulation. We find that TLR4 signaling in macrophages uniquely engages transcription factor IRF1, which facilitates opening of ISG loci for transcription. This study provides a critical mechanistic basis for lineage-specific TLR responses and uncovers IRF1 as a master epigenetic regulator for the ISG transcriptional program in human macrophages.
2021-03-16 | GSE147308 | GEO