ScRNA-seq of AAV-scramble or AAV-shBicd2 infected mice livers under Con A-induced acute autoimmune hepatitis
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE276168 | GEO | 2024/09/07
REPOSITORIES: GEO
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Project description:To explore the effect of Bicd2 in ConA-induced acute autoimmune hepatitis, we conducted RNA transcriptome profiling of plko-scramble or shBicd2 plasmid hydrodynamic-injected mice livers in response to ConA injection.
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Project description:Autoimmune hepatitis is an interface hepatitis characterized by the progressive destruction of the liver parenchyma, the cause of which is still obscure. Interleukin (IL)-17A is a major driver of autoimmunity, which can be produced by innate immune cells against several intracellular pathogens. Here, we investigated the involvement of IL-17A in a mice model of immune-mediated hepatitis with the intestine exposed to Salmonella typhimurium. Our results showed more severe Concanavalin (Con) A-induced liver injury and gut microbiome dysbiosis when the mice were treated with a gavage of S. typhimurium. Then the Natural Killer (NK) T cells were over-activated by the accumulated IL-17A in the liver in the Con A and S. typhimurium administration group. IL-17A could activate NKT cells by inducing CD178 expression via IL-4/STAT6 signaling. Furthermore, via the portal tract, the laminae propria mucosal-associated invariant T (MAIT) cell-derived IL-17A could be the original driver of NKT cells’ over-activation in intragastric administration of S. typhimurium and Con A injection. In IL-17A deficient mice, Con A-induced liver injury and NKT cells activation was alleviated. However, when AAV-sh-mIL-17a was used to specifically knock down IL-17A in liver, it seemed that hepatic IL-17a knock down did not significantly influence the liver injury. Our results suggested that, under Con A-induction, laminae propria MAIT-derived IL-17A activated hepatic NKT, and this axis could be a therapeutic target in autoimmune liver disease.
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Project description:The etiology of autoimmune hepatitis is poorly understood but likely involves Th1 cells producing IFN-γ. BALB/c background TGF-β1-/- mice rapidly develop fulminant Th1-mediated autoimmune hepatitis. Our aims are to profile liver gene expression in TGF-β1-/- mice, to identify gene expression pathways dependent on IFN-γ as possible targets for rational therapy, and to test potential targets directly in vivo in mice. Keywords: Comparative analysis of gene expression in livers of WT, TGFB1 & IFN knockout mice DNA microarray analyses were applied to liver RNA from TGF-β1-/- mice, TGF-β1-/- /IFN-γ-/- mice, and TGF-β1+/+ littermate controls. 3 mice from each group were analyzed in this study.
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Project description:We report the application of Illumina paired-end RNA-seq approach for transcriptome of brain tissue in mice. By removing sequence-dependent bias and amplification noise using UMI-tools. The mapped reads of each sample were assembled using StringTie. After the final transcriptome was generated, StringTie and edgeR was used to estimate the expression levels of all transcripts. By obtaining a total of million paired-end reads of sequence from cerebral cortex tissue, we generated transcriptome profiles of mouse ischemic cortex in sham, 24 h after focal ischemia, 28 d after focal ischemia, with or without neuron-specific knockdown of TIPARP, respectively. We found 2017 differentially expressed genes (DEGs) between Sham+AAV-SYN-shRNA-Con and tMCAO+AAV-SYN-shRNA-Con group, and 516 DEGs between tMCAO+AAV-SYN-shRNA-Con and tMCAO+AAV-SYN-shRNA-TIPARP group at 24 h after stroke. In addition, we found 487 DEGs between Sham+AAV-SYN-shRNA-Con and tMCAO+AAV-SYN-shRNA-Con group, and 192 DEGs between tMCAO+AAV-SYN-shRNA-Con and tMCAO+AAV-SYN-shRNA-TIPARP group at 28 d after stroke. This study provides a detailed analysis of the underlying mechanisms of neuron-specific knockdown of TIPARP in neuronal injury and long-term effect, with biologic replicates, generated by RNA-seq technology.
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Project description:Myeloid-derived suppressor cells (MDSC) represent a heterogeneous population of immature myeloid cells that accumulate in blood, liver, spleen and tumors upon chronic inflammation and tumor development in patients and mice. Acute hepatitis is characterized by a fast infiltration of inflammatory cells in the liver and increased enzymatic activity at this organ that could lead into liver fibrosis and cirrhosis. We have studied the biology of hepatic MDSC in acute hepatitis. Unexpectedly, hepatic MDSC, which accumulate in the liver of mice bearing subcutaneous tumors, failed to suppress inflammatory responses upon Con A injection, but instead were responsible for exacerbating acute liver damage. Phenotypic, genetic and functional studies demonstrated rapid changes of hepatic MDSC from a suppressor phenotype into a pro-inflammatory subset as early as 3 hours after Con A injection. An increase in the expression of pro-inflammatory cytokines, costimulatory molecules such as CD80, CD86 and CD40 along with a loss of suppressor function was noticed in mice upon Con A treatment. These changes were CD40-dependent and not found in CD40-/- MDSC. Interestingly, CD40 ligation of human MDSC in vitro resulted in down-regulation of arginase I expression and suppressor function. Finally, blockade of ROS production in hepatic MDSC ameliorated hepatocyte damage suggesting that MDSC mediated toxicity was ROS dependent. We believe that these findings reflect how MDSC plasticity can be modulated to promote inflammation, opening a new path for therapies targeting innate suppressive cells in cancer patients. EL4 tumors were established in C57BL/6 mice, then mice were injected either with PBS (n=3) or 12.5mg/kg Con A (n=3). Three hours later mice were sacrificed, liver CD11b+Gr-1+ cells were sorted and samples were processed for gene expression analysis.
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