Single cell RNA sequencing study of Lung epithelial cells with Il33 KO cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA739467 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14867882_1.fastq.gz | Fastqsanger.gz | |||
| SRR14867882_2.fastq.gz | Fastqsanger.gz | |||
| SRR14867883_1.fastq.gz | Fastqsanger.gz | |||
| SRR14867883_2.fastq.gz | Fastqsanger.gz | |||
| SRR14867884_1.fastq.gz | Fastqsanger.gz |
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Project description:Single cell ATAC-seq study of Lung epithelial cells with Il33 KO cells
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Project description:Epithelial cells are charged with protection at barrier sites, but whether this normally beneficial response might sometimes become dysfunctional still needs definition. Here we identify a pattern of imbalance marked by basal epithelial cell growth and differentiation that replaces normal airspaces in a mouse model of progressive post-viral lung disease due to Sendai virus. Single-cell and lineage-tracing technologies identify a distinct subset of basal epithelial stem cells (basal- ESCs) that extend into gas-exchange tissue to form long-term bronchiolar-alveolar remodeling regions. Moreover, this cell subset is selectively expanded by crossing a cell growth and survival checkpoint linked to the nuclear-localized alarmin IL-33 that is independent of IL-33-receptor signaling and instead connected to autocrine chromatin accessibility. This mechanism creates an activated stem-progenitor cell lineage with potential for physiological or pathological function. Thus, conditional loss of Il33 gene function in basal epithelial cells disrupts homeostasis of the epithelial barrier at skin and gut sites but also markedly attenuates post-viral disease in the lung based on down-regulation of remodeling and inflammation. We thereby identify a basal-ESC strategy to deploy innate-immune machinery that appears to overshoot the primordial goal of self- defense. The findings reveal new targets to stratify and correct chronic and often deadly post-viral disease.
2021-07-29 | GSE178711 | GEO
Project description:Epithelial cells are charged with protection at barrier sites, but whether this normally beneficial response might sometimes become dysfunctional still needs definition. Here we identify a pattern of imbalance marked by basal epithelial cell growth and differentiation that replaces normal airspaces in a mouse model of progressive post-viral lung disease due to Sendai virus. Single-cell and lineage-tracing technologies identify a distinct subset of basal epithelial stem cells (basal- ESCs) that extend into gas-exchange tissue to form long-term bronchiolar-alveolar remodeling regions. Moreover, this cell subset is selectively expanded by crossing a cell growth and survival checkpoint linked to the nuclear-localized alarmin IL-33 that is independent of IL-33-receptor signaling and instead connected to autocrine chromatin accessibility. This mechanism creates an activated stem-progenitor cell lineage with potential for physiological or pathological function. Thus, conditional loss of Il33 gene function in basal epithelial cells disrupts homeostasis of the epithelial barrier at skin and gut sites but also markedly attenuates post-viral disease in the lung based on down-regulation of remodeling and inflammation. We thereby identify a basal-ESC strategy to deploy innate-immune machinery that appears to overshoot the primordial goal of self- defense. The findings reveal new targets to stratify and correct chronic and often deadly post-viral disease.
2021-07-29 | GSE178517 | GEO
Project description:Focal adhesion kinase (FAK) is required for the expression of pro-inflammatory genes that inhibit anti-tumour immunity. Here, we show a novel and crucial role for the dual-function cytokine IL33 in FAK-dependent immune evasion. Specifically, nuclear FAK is required for the expression of IL33, the chemokine Ccl5 and the soluble form of the IL33 receptor, sST2, which are required for evasion of CD8+ T-cell-mediated anti-tumour immunity. Mechanistically, nuclear IL33 associates with FAK and a network of chromatin modifiers and transcriptional regulators, including Taf9, WDR82 and BRD4, while sST2 likely negates effects of IL33 secreted into the tumour microenvironment by infiltrating host immune cells. Finally, protein interaction network analysis implies that nuclear FAK–IL33 complexes impact on transcription factors that regulate NFkB and chemokines like Ccl5 downstream. Our data therefore provide new mechanistic insight into how FAK controls the tumour immune environment via a FAK–IL33/sST2 pathway and demonstrate a novel role for nuclear IL33 downstream of FAK as a component of transcription regulatory complexes that critically modulate anti-tumour immunity.
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Project description:IL33 is an alarmin protein that is known to be released by epithelial cells as a response to damage. There is also evidence that dendritic cells express IL33, however its function in these cells is not well understood. To investigate the distinct function of IL33 in dendritic cells, deep sequencing of mRNA transcripts was conducted on FACS sorted DCs in mice lacking Il33 expression in CD11c expressing cells compared to control mice.
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Project description:Lung epithelial cells produce alarmins that promote allergic inflammation, however, the molecular mechanisms that regulate alarmin expression and production have not been fully elucidated. We constructed an integrated single-cell RNA-seq atlas of murine airways, lung, and vagal nerves, which we use to characterize novel lung cell subsets and infer intercellular interactions, including an interaction between podoplanin (PDPN) on alveolar epithelial cells and C-type Lectin-like Receptor-2 (CLEC-2/Clec1b) on alveolar macrophages that controls the expression of IL-33. Clec1b-/- mice spontaneously develop allergic airway inflammation with increased Il33 expression in alveolar epithelial type 2 (AT2) cells and airway-associated fibroblasts; this airway inflammation is ameliorated by co-deletion of the IL-33 receptor, Il1rl1 (ST2). Myeloid cell-specific deletion of Clec1b and acute blockade of endogenous CLEC-2:PDPN interactions in vivo also promote type 2 immune responses in airway inflammation. Organoid experiments reveal that the regulation of AT2 Il33 expression by CLEC-2:PDPN interactions is directly mediated by alveolar macrophages. Single-cell characterization of house dust mite (HDM)-induced asthma reveals a smaller population of Clec1b expressing alveolar macrophages and increased Il33 expression by AT2 cells. Thus, our study has identified the CLEC-2:PDPN pathway as an important regulator of epithelial alarmin production and induction of type 2 immunity.
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Project description:TH2 and innate lymphoid cells 2 (ILC2) can stimulate tumor growth by secreting pro-tumorigenic cytokines such as IL4, IL5 and IL13. However, the mechanisms by which type 2 immune cells traffic to the tumor microenvironment (TME) are unknown. Here, in pancreatic ductal adenocarcinoma (PDAC), we show that oncogenic KrasG12D (Kras*) increases the expression of IL33 in cancer cells, which upon secretion recruits and activates the TH2 and ILC2. Correspondingly, cancer cell-specific deletion of IL33 reduces TH2 and ILC2 recruitment and promotes tumor regression. Unexpectedly, we discovered that the cellular release of IL33 into the TME is dependent on the intratumoral fungal mycobiome. Genetic deletion of IL33 or anti-fungal treatment decreases TH2 and ILC2 infiltration and increases survival. Consistent with these murine data, high IL33 expression is observed in approximately 20% of human PDAC, and expression is mainly restricted to cancer cells. These data expand our knowledge of the mechanisms driving PDAC tumor progression and identifies therapeutically targetable pathways involving intratumoral mycobiome-driven secretion of IL33.
2022-03-01 | GSE190103 | GEO
Project description:We report the RNAseq of mouse pancreatic cancer cell lines with Kras ON vs Kras OFF. TH2 and innate lymphoid cells 2 (ILC2) can stimulate tumor growth by secreting pro-tumorigenic cytokines such as IL4, IL5 and IL13. However, the mechanisms by which type 2 immune cells traffic to the tumor microenvironment (TME) are unknown. Here, in pancreatic ductal adenocarcinoma (PDAC), we show that oncogenic KrasG12D (Kras*) increases the expression of IL33 in cancer cells, which upon secretion recruits and activates the TH2 and ILC2. Correspondingly, cancer cell-specific deletion of IL33 reduces TH2 and ILC2 recruitment and promotes tumor regression. Unexpectedly, we discovered that the cellular release of IL33 into the TME is dependent on the intratumoral fungal mycobiome. Genetic deletion of IL33 or anti-fungal treatment decreases TH2 and ILC2 infiltration and increases survival. Consistent with these murine data, high IL33 expression is observed in approximately 20% of human PDAC, and expression is mainly restricted to cancer cells. These data expand our knowledge of the mechanisms driving PDAC tumor progression and identifies therapeutically targetable pathways involving intratumoral mycobiome-driven secretion of IL33.
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