Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1009041 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25756625_1.fastq.gz | Fastqsanger.gz | |||
| SRR25756625_2.fastq.gz | Fastqsanger.gz | |||
| SRR25756626_1.fastq.gz | Fastqsanger.gz | |||
| SRR25756626_2.fastq.gz | Fastqsanger.gz | |||
| SRR25756627_1.fastq.gz | Fastqsanger.gz |
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Project description:The efficacy of costimulation blockade (CTLA4Ig/belatacept) in transplantation is reduced by an increased incidence of T cell-mediated rejection, which also persists after induction therapy with anti-thymocyte globulin (ATG). Herein, we investigate why ATG fails to prevent costimulation blockade-resistant rejection and how this barrier can be overcome. ATG did not prevent graft rejection in a murine heart transplant model of CTLA4Ig therapy and induced a pro-inflammatory cytokine environment. While ATG improved the balance between Tregs and effector T cells in the peripheral compartment, it had no such effect within cardiac allografts, which showed signs of inflammation. Neutralizing IL-6 alleviated inflammation, increased intragraft Treg frequencies long-term, and enhanced intragraft IL-10 and Th2 cytokine expression. IL-6 blockade together with ATG led to long-term, rejection-free heart graft survival under CTLA4Ig therapy. Combining ATG with IL-6 blockade prevents costimulation blockade-resistant rejection, thereby eliminating a major impediment to clinical use of costimulation blockers in transplantation.
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Project description:The efficacy of costimulation blockade (CTLA4Ig/belatacept) in transplantation is reduced by an increased incidence of T cell-mediated rejection, which also persists after induction therapy with anti-thymocyte globulin (ATG). Herein, we investigate why ATG fails to prevent costimulation blockade-resistant rejection and how this barrier can be overcome. ATG did not prevent graft rejection in a murine heart transplant model of CTLA4Ig therapy and induced a pro-inflammatory cytokine environment. While ATG improved the balance between Tregs and effector T cells in the peripheral compartment, it had no such effect within cardiac allografts, which showed signs of inflammation. Neutralizing IL-6 alleviated inflammation, increased intragraft Treg frequencies long-term, and enhanced intragraft IL-10 and Th2 cytokine expression. IL-6 blockade together with ATG led to long-term, rejection-free heart graft survival under CTLA4Ig therapy. Combining ATG with IL-6 blockade prevents costimulation blockade-resistant rejection, thereby eliminating a major impediment to clinical use of costimulation blockers in transplantation.
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Project description:Obesity is associated with severe, difficult to control asthma, and increased airway oxidative stress. Mitochondrial reactive oxygen species (mROS) are an important source of oxidative stress leading us to hypothesize that targeting mROS in obese allergic asthma might be an effective treatment strategy. Using a mouse model of house dust mite (HDM) induced allergic airway disease in mice fed a low- (LFD) or high-fat diet (HFD), and the mitochondrial antioxidant MitoQuinone (MitoQ); we investigated the effects of obesity and mROS on airway inflammation, remodelling and airway hyperreactivity (AHR). HDM induces airway inflammation, remodelling and hyperreactivity in both lean and obese mice. Obese allergic mice showed increased lung tissue eotaxin levels, airway tissue eosinophilia and AHR when compared to lean allergic mice. MitoQ reduced markers of airway inflammation, remodelling and hyperreactivity in both lean and obese allergic mice, and tissue eosinophilia in obeseHDM mice. mROS regulates cell signalling by protein oxidation of multiple downstream targets: MitoQ reduced HDM-induced cysteine-sulfenylation of several proteins including those involved in the unfolded protein response (UPR). In summary, mROS mediates the development of allergic airway disease and hence MitoQ might be effective for the treatment for asthma, and specific features of obese asthma.
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Project description:Arctigenin (ATG) is a major component of Fructus Arctii, which as a traditional herbal remedy reduced proteinuria in diabetic patients. However, whether ATG specifically provided renoprotection in DKD was not known. Here we report that ATG administration is sufficient to attenuate proteinuria and podocyte injury in mouse models of diabetes. Transcriptomic analysis of diabetic mouse glomeruli showed that cell adhesion and inflammation are two key pathways affected by ATG treatment, and mass spectrometry analysis identified protein phosphatase 2A (PP2A) as one of the top ATG-interacting proteins in renal cells. Enhanced PP2A activity by ATG reduces p65 NF-κB-mediated inflammatory response and high glucose-induced migration in cultured podocytes via its interaction with Drebrin-1. Importantly, podocyte-specific Pp2a deletion in mice exacerbates DKD injury and abrogates the ATG-mediated renoprotection. Collectively, our results clearly demonstrate a renoprotective mechanism of ATG via PP2A activation and establish PP2A as a potential target for DKD progression.
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