Relevance of IL-3 for lung transcriptomic response in murine sepsis followed by HSV infection
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA930483 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23310504.fastq.gz | Fastqsanger.gz | |||
| SRR23310505.fastq.gz | Fastqsanger.gz | |||
| SRR23310506.fastq.gz | Fastqsanger.gz | |||
| SRR23310507.fastq.gz | Fastqsanger.gz | |||
| SRR23310508.fastq.gz | Fastqsanger.gz |
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Project description:To investigate the importance of IL-3 during the pulmonary response to HSV infection after initial polymicrobial sepsis
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Project description:Adoptive transfer of T cells from wild-type (WT) mice to IL-17A-/- mice or T cells from IL-17A-/- mice to Rag-/- mice induced CNS demyelination in infected mice. Adoptive T cell experiments suggest that both T cells and non-T cells expressing IL-17A contribute to HSV-IL-2-induced CNS demyelination with no difference in the severity of demyelination between the two groups of IL-17A producing cells. IL-6, IL-10, or TGFβ did not contribute to CNS demyelination in infected mice. Transcriptome analysis between IL-17A-/- brain and spinal cord of infected mice with and without T cell transfer from WT mice revealed that “neuron projection extension involved in neuron projection guidance” and “ensheathment of neurons” pathways were associated with CNS demyelination. Collectively, the results indicate the importance of IL-17A in CNS demyelination and the possible involvement of more than three of IL-17 receptors in CNS demyelination
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Project description:The aim of this study was to compare the signaling cascades initiated by the two closely related cytokines IL-2 and IL-15. Considering the relevance of protein tyrosine phosphorylation in signal transduction, in order to quantify changes in protein phosphorylation in response to IL-2 and IL-15, we combined triple SILAClabeling of leukemic T-cells with phosphotyrosine (pY)-specific antibody-based protein enrichment followed by mass spectrometry (MS) analysis. Following the strategy described above, we managed to decipher in detail the complex signaling networks triggered by IL-2 and IL-15. Interestingly, a large number of components of the three main signaling pathways known to be initiated in response to the interleukins (JAK/STAT; RAS/MAPK; PI3K/AKT) were identified.
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Project description:Inflammation resolution is critical for sepsis induced acute lung injury (ALI) recovery. Interleukin-36 receptor (IL-36R) is a potent anti-inflammatory factor. However, its role in ALI resolution remains unclear. We investigated the effects of IL-36R during the ALI resolution process in a murine cecal ligation and puncture (CLP)-induced ALI model. Knockout IL-36R signaling aggravates CLP-induced lung injury, as manifested by elevated bacterial load and increased neutrophils recruitment to the lung. Thereafter, we used IL-36R knockout mice to discern the source cell of IL-36R during ALI. We found that IL-36R is predominantly generated by epithelial cells during the ALI process. Furthermore, we sorted lung epithelial cells on the ALI process. IL-36R-specific loss in epithelial cells leads to apoptosis through NF-κB pathway. Together, our findings identify molecules that are likely involved in sepsis induced lung injury that may inform biomarker and therapeutic development.
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Project description:The aim of this study was to compare the signaling cascades initiated by the two closely related cytokines IL-2 and IL-15. Considering the relevance of protein tyrosine phosphorylation in signal transduction, in order to quantify changes in protein phosphorylation in response to IL-2 and IL-15, we combined triple SILAClabeling of leukemic T-cells with phosphotyrosine (pY)-specific antibody-based protein enrichment followed by mass spectrometry (MS) analysis. Following the strategy described above, we managed to decipher in detail the complex signaling networks triggered by IL-2 and IL-15. Interestingly, a large number of components of the three main signaling pathways known to be initiated in response to the interleukins (JAK/STAT; RAS/MAPK; PI3K/AKT) were identified.
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