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ScRNA-sequencing of mesenchymal cells and immune cells sorted from the lung of PBS or HDM challenged mice

ABSTRACT: scRNA-sequencing of mesenchymal cells and immune cells sorted from the lung of PBS or HDM challenged mice

PROVIDER: PRJNA928691 | ENA |

REPOSITORIES: ENA

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			Action	DRS
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	SRR23253200.fastq.gz	Fastqsanger.gz
	SRR23253201.fastq.gz	Fastqsanger.gz
	SRR23253202.fastq.gz	Fastqsanger.gz
	SRR23253203.fastq.gz	Fastqsanger.gz

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scRNA-sequencing of mesenchymal cells and immune cells sorted from the lung of PBS or HDM challenged mice

Project description:We compared the transcriptomes of mesenchymal cells and immune cells in mice sensitized and challenged with house dust mite (HDM) extracts and those in control PBS-treated mice, using single cell RNA-seq (scRNA-seq). Data with mesenchymal cells and data with immune cells were obtained from separate experiments. For scRNA-seq of mesenchymal cells, each sample was pooled from cells from 3 mice and 2 different samples per group (for a total of 6 mice) were used. For scRNA-seq of immune cells, each sample was from cells of one individual mouse.

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Transcriptomic analysis in airway epithelial cells in HDM-sensitized STAT3-WT and STAT3-cKO mice

Project description:Purpose: To elucidate the roles of airway epithelial STAT3 in allergic airway inflammation. Method: Doxycycline-induced airway epithelial cells-specific STAT3-deficient mice (STAT3-cKO) and their genetic control mice (STAT3-WT) were sensitized intratracheally twice with house dust mite (HDM) extract or PBS at a 7-day interval. Airway epithelial cells were isolated by a cell sorter 48 h after the last senstization. N=2 each. Results: Using an optimized data analysis workflow, 206 transcripts showed differential expression between HDM-treated STAT3-WT and STAT3-cKO with adjusted p value <0.05.

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Alteration in gene expression in the lung following neonatal RSV infection

Project description:mRNA expression data from BALB/c mice which were infected intranasally with Respiratory Syncytial Virus (or Hep-2 cell lysate control) at 1 week old and challenged with PBS or house dust mite (HDM) extract as adults. Experimental groups: RH – neonatal RSV, adult HDM, RP – neonatal RSV, adult PBS, HH – neonatal Hep-2, adult HDM and HP – neonatal Hep-2, adult PBS.

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Project description:Our study investigates the activation and transcriptional programming of primary skin cells (FACS-purified Langerhans cells and single cell analysis of the whole biopsy) from patients with atopic dermatitis (n=22, nr = rensponding, nnr=nonresponding), exposed to a control or HDM patch test. 6 mm biopsies were taken from control and HDM patch test site 48h post application.

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Project description:Analysis of gene expression profile in peritoneal macrophage extracted from LPS or PBS challenged DUSP3-/- and WT mice. DUSP3 deletion protects mice from sepsis and endotoxemia. We performed a microarray analysis to get insights into the differentially regulated pathways between WT and KO under inflammatory conditions. Total RNA obtained from isolated peritoneal macrophages isolated from DUSP3-/- and WT mice 36 hours after challenging them in vivo with PBS or with 6mg/kg of LPS.

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Single cell gene expression profile of bronchoalveolar lavage fluid (BALF) cells from Apoa1-/- and Apoa1+/+ mice challenged with LPS and house dust mite

Project description:Neutrophils play important roles in inflammatory airway diseases. Here, we assessed whether apolipoprotein A-I (apoA-I) modifies neutrophil heterogeneity as part of the mechanism by which it attenuates acute airway inflammation. Neutrophilic airway inflammation was induced by daily intranasal administration of LPS plus house dust mite (LPS+HDM) to Apoa1-/- and Apoa1+/+ mice for 3 days. Single cell RNA sequencing was performed on cells recovered in bronchoalveolar lavage fluid (BALF) on day 4. Unsupervised profiling identified 10 clusters of neutrophils in BALF from Apoa1-/- and Apoa1+/+ mice. LPS+HDM-challenged Apoa1-/- mice had an increased proportion of the Neu4 neutrophil cluster that expressed S100a8, S100a9, and Mmp8, and had high maturation, aggregation, and TLR4 binding scores. There was also an increase in the Neu6 cluster of immature neutrophils, whereas neutrophil clusters expressing interferon-stimulated genes were decreased. An unsupervised trajectory analysis showed that Neu4 represented a distinct lineage in Apoa1-/- mice. LPS+HDM-challenged Apoa1-/- mice also had an increased proportion of recruited airspace macrophages, which was associated with a reciprocal reduction in resident airspace macrophages. Increased expression of a common set of pro-inflammatory genes, S100a8, S100a9, and Lcn2, was present in all neutrophils and airspace macrophages from LPS+HDM-challenged Apoa1-/- mice. Apoa1-/- mice have increases in specific neutrophil and macrophage clusters in the lung during acute inflammation mediated by LPS+HDM, as well as enhanced expression of a common set of pro-inflammatory genes. This suggests that modifications in neutrophil and macrophage heterogeneity contribute to the mechanism by which apoA-I attenuates acute airway inflammation.

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