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Active Mycobacterium tuberculosis regulatory networks from alveolar macrophages of in vivo mouse infection uncovered by Path-seq

ABSTRACT: Active Mycobacterium tuberculosis regulatory networks from alveolar macrophages of in vivo mouse infection uncovered by Path-seq

PROVIDER: PRJNA478391 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7448503_1.fastq.gz	Fastqsanger.gz
	SRR7448503_2.fastq.gz	Fastqsanger.gz
	SRR7448504_1.fastq.gz	Fastqsanger.gz
	SRR7448504_2.fastq.gz	Fastqsanger.gz
	SRR7448505_1.fastq.gz	Fastqsanger.gz

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Active Mycobacterium tuberculosis regulatory networks from in vitro infection of mouse macrophages uncovered by Path-seq

Project description:Active Mycobacterium tuberculosis regulatory networks from in vitro infection of mouse macrophages uncovered by Path-seq

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Active Mycobacterium tuberculosis regulatory networks from alveolar macrophages of in vivo mouse infection uncovered by Path-seq

Project description:Transcriptional profiling of Mycobacterium tuberculosis mRNA enriched from host-pathogen samples from in vivo alveolar macrophages (Mus musculus).

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Active Mycobacterium tuberculosis regulatory networks from in vitro infection of mouse macrophages uncovered by Path-seq

Project description:Transcriptional profiling of Mycobacterium tuberculosis mRNA enriched from host-pathogen samples from in vitro bone marrow derived macrophages (Mus musculus).

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Project description:PATH is a research study for cancer survivors to help participants to become more active. Studies suggested an association between inactivity and cancer. The investigators created new novel ways and technologies that may help participants to become more active. The three methods the investigators are studying are: 1) participant become active on her/his own; educational material will be provided; 2) working with a programmed health coach over the phone via text messages; and 3) using digital voice assist to help participant become more active. The digital voice assist will be delivered via Amazon Alexa on Echo speaker (it is the famous intelligent voice that you see in superball commercial by Alec Baldwin). This study is funded by the State of Maryland.

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Transcriptomic analysis of control lung alveolar type 2 cells and constitutively active-BMPR1a overexpressing alveolar type 2 cells

Project description:Transcriptomic analysis of control lung alveolar type 2 cells and constitutively active-BMPR1a overexpressing alveolar type 2 cells

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Transcriptomic analysis of control lung alveolar type 2 cells and constitutively active-BMPR1a overexpressing alveolar type 2 cells

Project description:The Bone Morphogenetic Protein (BMP) signaling pathway functions in lung development and the regeneration of adult tracheal epithelium from basal stem cells. Here, we explore its role in the alveolar region, where Type 2 epithelial cells (AT2s) and Pdgfrα+ Type 2 - associated stromal cells (TASCs) are components of the stem cell niche. We utilize both organoid assays and in vivo alveolar regrowth after pneumonectomy (PNX) - a process requiring proliferation of AT2s and differentiation into Type 1 cells (AT1). BMP signaling is normally active in AT2s and TASCs, transiently declines post-PNX, and is restored during differentiation of AT2s to AT1s. In organoids, BMP4 inhibits AT2 proliferation, while antagonists promote AT2 self-renewal at the expense of differentiation. Gain and loss-of function genetic manipulation reveals that loss of BMP signaling in AT2s after PNX allows their self-renewal but significantly reduces differentiation into AT1s; conversely, increased BMP signaling promotes AT1 formation. The transcriptome analysis of control AT2s and AT2s overexpressing constitutively active-Bmpr1a reveals that 119 genes are upregulated more than two-fold following enhancing BMP signaling. Of these genes, 10 % are normally preferentially expressed in AT1 cells. Of the 25 genes downregulated more than two-fold, 28 % are preferentially expressed in AT2s.

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Cigarette smoking alters mRNA expression in human alveolar macrophages

Project description:Alveolar macrophages from never smokers and active smokers were isolated by bronchoalveolar lavage and gene expression was measured. Chronic cigarette smoke exposure, as occurs in smoker's lungs, leads to significant changes in gene expression. Of note, RNA was isolated immediately following bronchoscopy. Alveolar macrophage levels were >95%. 4 never smokers and 4 active smokers were recruited for the study. After bronchoalveolar lavage and RNA isolation, gene expression was measured using Affymetrix Human Exon 1.0 ST arrays.

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Immunoproteasome dysfunction augments alternative polarization of alveolar macrophages

Project description:The proteasome is a central regulatory hub for intracellular signaling by degrading numerous signaling mediators. Immunoproteasomes are specialized types of proteasomes known to be involved in shaping adaptive immune responses, but their role for innate immune signaling is elusive. Here, we analyzed immunoproteasome function for polarization of alveolar macrophages which are highly specialized tissue macrophages of the alveolar surface of the lung. Classical activation (M1 polarization) of primary alveolar macrophages by LPS/IFNÎ³ transcriptionally induced all three immunoproteasome subunits LMP2, LMP7, and MECL-1. In contrast, IL-4 triggered alternative (M2) activation was accompanied by posttranscriptional upregulation of LMP2 and LMP7. Accordingly, immunoproteasome activity increased in M1 cells, and to some extent under M2 conditions. Analyzing the polarization capability from LMP7 deficient mice revealed no effect on the LPS/IFNÎ³ triggered M1 profile, but uncovered a distorted M2 profile for IL-4 stimulated LMP7-/- alveolar macrophages as characterized by increased M2 marker gene expression and CCL17 cytokine release. This shift in immunoproteasome-dependent M2 polarization was accompanied by amplified AKT/STAT6 activation and IRF4 expression in LMP7-/- alveolar macrophages. IL-13 stimulation of LMP7 deficient cells induced a similar M2 skewed profile and IL4RÎ± protein expression was generally elevated in LMP7-/- alveolar macrophages, indicating that amplified IL4R signaling in immunoproteasome defective cells may contribute to augmented M2 polarization. Importantly, treatment with an LMP7-specific proteasome inhibitor recapitulated the findings of genetic LMP7 inactivation. Our results thus suggest a novel role of immunoproteasome function for regulating innate immune function of macrophages by limiting IL4R expression and signaling. Expression data of M0 and M2 macrophages derived from Lmp7 k.o. and control animals

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YAP regulates NFI/KLF5 transcriptional and epigenetic networks directing alveolar epithelial cell differentiation

Project description:YAP regulates NFI/KLF5 transcriptional and epigenetic networks directing alveolar epithelial cell differentiation

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