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CoMtb alters the immune landscape following Mtb infection [B6 Sp140-/- scRNA-Seq]

ABSTRACT: To gain further insights into lesion development and effects of CoMtb on immune responses during infection. we performed single-cell RNA sequencing (scRNAseq) and flow cytometry analysis of lungs from Mtb-infected B6 Sp140-/- mice with and without CoMtb at 10 days after CD infection. We found that CoMtb induces rapid recruitment and activation of T cells. macrophage activation. and diminished late neutrophil responses.

ORGANISM(S): Mus musculus

PROVIDER: GSE266432 | GEO | 2024/06/18

REPOSITORIES: GEO

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CoMtb alters the immune landscape following Mtb infection [B6 Sp140-/- scRNA-Seq]

Project description:CoMtb alters the immune landscape following Mtb infection [B6 Sp140-/- scRNA-Seq]

| PRJNA1107174 | ENA

CoMtb alters the immune landscape following Mtb infection [B6 scSCRNAseq]

Project description:To characterize the influence of CoMtb on immune responses during infection, we performed single-cell RNA sequencing (scRNAseq) and flow cytometry analysis of lungs from Mtb-infected C57Bl/6 mice with and without CoMtb immediately pre-infection and at 10, 17 and 34 days after conventional dose (50-100 CFU) Mtb infection. We found that CoMtb induces rapid recruitment and activation of T cells, macrophage, and diminished late neutrophil responses.

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CoMtb alters the immune landscape following Mtb infection [C3H scRNAseq]

Project description:To gain further insights into lesion development and effects of CoMtb on immune responses during infection. we performed single-cell RNA sequencing (scRNAseq) and flow cytometry analysis of lungs from Mtb-infected animals with and without CoMtb immediately pre-infection and at 10. 17 and 34 days after CD infection. We found that CoMtb induces rapid recruitment and activation of T cells. macrophage activation. and diminished late neutrophil responses.

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CoMtb alters the immune landscape following Mtb infection [B6 scSCRNAseq]

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Single-cell gene expression analysis of pulmonary immune cells from BCG-vaccinated and CoMtb mice [scRNAseq]

Project description:The aim of this study was to measure effect of BCG vaccination or contained Mtb infection (CoMTB) on the expression profile of pulmonary immune cells.

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Gene expression analysis of alveolar macrophages from BCG-vaccinated and CoMtb mice stimulated ex vivo [exvivoRNAseq]

Project description:The aim of this study was to measure the response of alveolar macrophages (AMs) from BCG-vaccinated mice and mice with CoMtb to LPS, PAM3CSK4, and Mtb stimulation ex vivo.

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CITE-seq analysis of Mycobacterium tuberculosis infected B6 and Sp140-deficient mouse lungs

Project description:Mycobacterium tuberculosis (Mtb) causes 1.5 million deaths annually. Active tuberculosis correlates with a neutrophil-driven type I interferon (IFN) signature, but the underlying cellular mechanisms remain poorly understood. We found that interstitial macrophages (IMs) and plasmacytoid dendritic cells (pDCs) are dominant producers of type I IFN during Mtb infection in mice and non-human primates, and pDCs localize near human Mtb granulomas. Depletion of pDCs reduces Mtb burdens, implicating pDCs in tuberculosis pathogenesis. During IFN-driven disease, we observe abundant DNA-containing neutrophil extracellular traps (NETs) known to activate pDCs. Single cell RNA-seq indicates that type I IFNs act on IMs to impair their responses to IFNg, a cytokine critical for Mtb control. Cell type-specific disruption of the type I IFN receptor suggests IFNs act on IMs to inhibit Mtb control. We propose pDC-derived type I IFNs, driven by NETs, act on IMs to drive bacterial replication, further neutrophil recruitment, and active tuberculosis disease.

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The antiviral nuclear body protein SP140 represses Ifnb1 transcript stabilization by the novel regulator RESIST [WT and SP140 KO RNA-seq]

Project description:Negative regulation of the antiviral cytokine IFN-I is critical to prevent host pathology, but is not fully understood. The highly conserved but understudied epigenetic reader and nuclear body protein SP140 represses IFN-I by an unknown mechanism. We describe the mechanism by which SP140 negatively regulates IFN-I, and include RNA-seq data of WT (B6) and SP140 KO BMMs untreated or treated with 100 ug/mL DMXAA for 8 hours in this dataset. We found that SP140 represses the expression of a novel positive regulator of IFN-I previously annotated as an annexin II receptor, which we rename RESIST (REgulated Stimulator of IFN-I via Stabilization of Transcript). RESIST promotes IFN-I mRNA stability by binding the CCR4-NOT mRNA deadenylase complex and blocking recruitment of the TTP family of RNA-binding proteins, which negatively regulate IFN-I mRNA stability, to CCR4-NOT. Mechanistically, RESIST uses N and C-terminal alpha-helices respectively to either dock to the CCR4-NOT complex or block TTP family binding. Our work reveals a new regulator of IFN-I and a new mechanism regulating IFN-I mRNA stability.

2024-08-28 | GSE269808 | GEO

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