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ABSTRACT:
PROVIDER: PRJNA1280697 | ENA |
REPOSITORIES: ENA
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Project description:Our findings demonstrate that XBP1 controls macrophage cGAS/STING/NLRP3 activation by regulating macrophage self-mtDNA cytosolic leakage via BNIP3-mediated mitophagy modulation, providing a novel target against liver fibrosis.
2025-06-17 | GSE206693 | GEO
Project description:Purpose: RNA-Seq has become a powerful tool for investigating transcriptional profiles in gene expression analysis, which would help to reveal the molecular mechanism of Clostridium perfringens type C infecting the piglets. In this study, we analyzed the transcriptome profiles of the spleen of piglets caused by Clostridium perfringens type Cens type C. Methods: 30 normal 7-day-old piglets (Y x L), without infecting Clostridium perfringens type C, Escherichia coli and Salmonella, were selected as experimental subjects. 25 piglets were randomly selected as the experimental group, which were disposed once a day for 5 days. Each piglet was dosed with 1 ml of bouillon culture-medium inoculated Clostridium perfringens type C at 37℃ for 16h, which approximate to 1 x109 CFU per ml. Then, 5 piglets were randomly selected as the control group (SC), which were taken the equal volume medium for 5 days.Based on total diarrhea scores, 25 piglets were ranked from high to low. The top and last five piglet were considered as sensitive group (SS) and resistant group (SR), respectively. Finally, spleen were collected and sequenced for lncRNA and mRNA. Results: RNA libraries constructed from spleen of piglets caused by Clostridium perfringens type C were sequenced. A total of 1,450,292,484 clean reads were generated. Among them, 2056 novel lncRNA transcripts corresponding to 1561 lncRNA genes were identified, including 1811 intergenic lncRNAs and 245 anti-sense lncRNAs. The identified spleen lncRNAs shared some characteristics, such as fewer exons and shorter length, with the lncRNAs in other animal. Notably, in pairwise comparisons between the libraries of spleen tissue at the different group, a total of 247 lncRNA and 2170 mRNA were differentially expressed (P < 0.05). Function analyses indicated that these differentially expressed lncRNAs and mRNAs play roles in defensing Clostridium perfringens type C, which were enriched in immune-related biological processes, such as the antigen processing and presentation, TNF signaling pathway, NF-kappa B signaling pathway, B cell receptor signaling pathway and MAPK signaling pathway. Conclusions: This study provides the information of spleen-related lncRNAs in swine diarrhea with Clostridium perfringens type C. We also analyzed all lncRNA’s genomic feature and expression. Bioinformatic analysis indicates that some lncRNAs participated in important biological processes associated with defeasing Clostridium perfringens type C, such as antigen processing and presentation, the MHC protein complex and regulation of autophagy.
2018-11-01 | GSE105797 | GEO
Project description:Purpose: The purpose of this study is to clarify the response of Clostridium perfringens ATCC 13124 to host polysaccharide. Methods: Clostridium perfringens ATCC 13124 cells were cultured anaerobically in a medium containing Minimal medium-like condition Poor + medium, medium in which hyaluronic acid or mucin was added to Poor + medium. Total RNA was extracted from bacterial cells by the Hot-Phenol method. Samples for RNA-seq were prepared according to the Illmina protocol available from the manufacturer. Array leads passed through quality filters were analyzed at the transcript isoform level using bowtie v 1.1.2. Results: Using the optimized data analysis workflow, we mapped about 50 million sequence leads per sample to the whole genome of Clostridium perfringens ATCC 13124. In addition, 2735 transcripts in C. perfringens ATCC 13124 were identified using a Bowtie aligner. Lead counts per genome were extracted from known gene annotations using the HTSeq program.
2024-07-29 | GSE240236 | GEO
Project description:Recombinant adenoviral vectors (rAds), derived from distinct species with different serotypes, are lead vaccine candidates against Ebola, HIV, Tuberculosis and Malaria based on their potent induction of T cell immunity in humans. Importantly, rAds vary in their ability to induce protective cellular immunity. Here, the in vivo mechanisms controlling potency of CD8 T cell responses were assessed after vaccination with human-, chimpanzee- and simian-derived rAds encoding SIV-Gag. After rAd vaccination, we quantified antigen (Ag) expression and performed expression profiling of innate immune response genes in the draining lymph node. The most potent rAds (human-derived rAd5 and chimpanzee-derived chAd3) induced high and persistent Ag expression with low innate gene activation, while the less potent rAds exhibited reduced Ag expression with robust innate gene activation associated primarily with interferon (IFN) signaling. Abrogation of type I IFN or stimulator of IFN genes (STING) signaling increased Ag expression and accelerated CD8 T cell response kinetics, but did not alter memory responses or protection. Thus, the magnitude of memory CD8 T cell immune responses induced by rAds correlates with Ag expression but is independent of IFN and STING. These findings provide criteria for optimal induction of protective CD8 T cell immunity with rAd vaccines.
2014-12-30 | GSE64548 | GEO
Project description:Phosphoproteomics show that the tumor suppressor kinase DAPK3 drives tumor-intrinsic immunity through the STING-IFNb pathway
2021-01-15 | MSV000086706 | MassIVE
Project description:Background and Aims: The activation of stimulator of interferon genes (STING) and NOD-like receptors protein 3 (NLRP3) inflammasomes-mediated pyroptosis signaling pathways represent two distinct central mechanisms in liver disease. However, the interconnection between these two pathways and the epigenetic regulation of the STING-NLRP3 axis in hepatocyte pyroptosis during liver fibrosis remain unknown and is the focus of this study. Approach and Results: Liver fibrosis was induced in Sting knockout, Gasdermin D (Gsdmd) knockout mice, and in mice with hepatocyte-specific Nlrp3 deletion. RNA-sequencing, metabolomics, epigenetic compound screening system, and chromatin immunoprecipitation were utilized. STING and NLRP3 inflammasome signaling pathways were activated in cirrhotic livers but were suppressed by Sting knockout. Sting knockout also ameliorated hepatic pyroptosis, inflammation, and fibrosis in the murine cirrhotic model. In vitro, STING induced pyroptosis in primary murine hepatocytes via activating the NLRP3 inflammasome. H3K4-specific histone methyltransferase WD repeat-containing protein 5 (WDR5) and DOT1-like histone H3K79 methyltransferase (DOT1L) were identified to regulate NLRP3 expression in STING-overexpressed AML12 hepatocytes. WDR5/DOT1L-mediated histone methylation enhanced interferon regulatory transcription factor 3 (IRF3) binding to the Nlrp3 promoter and promoted STING-induced Nlrp3 transcription in hepatocytes. The RNA-sequencing and metabolomics analysis in murine livers and primary hepatocytes showed that metabolic reprogramming might participate in NLRP3-mediated hepatocyte pyroptosis and liver fibrosis. Moreover, hepatocyte-specific Nlrp3 deletion and downstream Gsdmd knockout attenuated hepatic pyroptosis, inflammation, and fibrosis in murine cirrhotic models. Conclusions: This study describes a novel epigenetic mechanism by which the STING-WDR5/DOT1L/IRF3-NLRP3 signaling pathway enhances hepatocyte pyroptosis and hepatic inflammation in liver fibrosis.
2023-09-18 | GSE217363 | GEO
Project description:Proteome analysis reveals that the tumor suppressor kinase DAPK3 drives tumor-intrinsic immunity through the STING-IFNb pathway Proteome
2021-01-15 | MSV000086708 | MassIVE
Project description:DNA sensing is a fundamental process in the immune system, including host defence against viruses. The DNA sensor cGAS synthesises 2’3’ cyclic GMP-AMP (cGAMP), a second messenger that activates STING, which subsequently induces innate immunity. cGAMP not only activates STING in the cell where it is produced but also transfers to other cells. Transporters, channels and pores including SLC19A1, the SLC46A family, P2X7, ABCC1 and volume-regulated anion channels (VRACs) release cGAMP into the extracellular space and/or import cGAMP into cells. Emerging evidence suggests these proteins are important in antiviral immunity. Here, we investigated whether viruses antagonise cGAMP transporters, channels and pores. We report that infection with multiple human viruses depleted cGAMP conduits from cells. This included herpes simplex virus 1 (HSV-1) that targeted the VRAC subunits LRRC8A and LRRC8C, as well as SLC46A2 and P2X7, for degradation. The HSV-1 protein UL56 was required and sufficient for these effects that were mediated at least partially by proteasomal turnover. UL56 thereby inhibited the cGAMP uptake via VRAC, SLC46A2 and P2X7. Taken together, we show that HSV-1 actively antagonises cGAMP transfer across the plasma membrane and propose this limits innate immunity by reducing cell-to-cell communication via the immunotransmitter cGAMP.
2024-04-15 | PXD043229 | Pride
Project description:A longstanding barrier in vaccinology has been the inability to reconcile potent mucosal immune activation with systemic tolerability, hindering adjuvant development for over a century. Here, we present NanoCF501, a nanoparticulate STING agonist engineered with respiratory-tuned, clinically safe polymers, which overcomes this fundamental limitation. When co-administered with a multivalent pan-β-coronavirus subunit vaccine, NanoCF501 at 1/20th the systemic adjuvant dose elicits coordinated mucosal-systemic immunity, inducing robust and durable cross-protective responses. These include mucosal secretory IgA and tissue-resident memory T cells alongside systemic neutralizing antibodies, memory B cells, and long-lived plasma cells persisting >12 months in murine models. Non-human primates validate the dual-axis mucosal-systemic coupling, while toxicology studies in rats demonstrate more than 18-fold safety margin and undetectable systemic exposure, underscoring translational viability. Mechanistic interrogation via single-cell transcriptomics reveals that NanoCF501 drives STING-dependent innate immune activation, orchestrating broad transcriptional reprogramming in lung antigen-presenting cells and efficient priming of adaptive T and B cell responses. Notably, NanoCF501 converts conventional quadrivalent influenza subunit vaccines into mucosal immunogenic formulations, demonstrating platform versatility. By integrating rational nanocarrier design with innate immune targeting, this work establishes a universal mucosal vaccination strategy with broad implications for pandemic preparedness and mucosal vaccinology.
2025-05-21 | GSE297387 | GEO