Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-Seq analysis of gene expression changes by wildtype and Nlrx1 deficient BEAS-2B airway epithelial cells in response to A. fumigatus viable conidia

ABSTRACT: Aspergillus fumigatus is an opportunistic fungal pathogen of the respiratory system that may cause invasive infection or an allergic response. Bronchial airway epithelial cells compromise the most abundant cell type of the pulmonary-air interface. Our recent findings suggest loss of Nlrx1 by BEAS-2B airway epithelial cells result in a hyper inflammatory response as well as decreased conidial processing. We challenged wildtype Nlrx1 deficient BEAS-2B cells with viable A. fumigatus AF293 conidia to identify early response differentially expressed genes and pathways between the two cell populations.

ORGANISM(S): Homo sapiens

PROVIDER: GSE144652 | GEO | 2023/01/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Time course RNA-Seq analysis of wildtype and Nlrx1 deficient bone marrow derived monocytoid dendritic cells indicate decision tree in response to A. fumigatus viable conidia

Project description:Aspergillus fumigatus is an opportunistic fungal pathogen of the respiratory system that may cause invasive infection or an allergic response. Monocytoid dendritic cells (moDCs) are a known recruited cell population during fungal colonization and are believed to be a critical player in balancing innate versus adaptive immune responses. We conducted an RNA-Seq time course analysis of moDCs challenged against A. fumigatus, to gain an appreciation of gene expression changes. We concurrently utilized Nlrx1 deficient moDCs as we have recently shown the importance of Nlrx1 during invasive pulmonary aspergillosis and shown the absence of Nlrx1 results in a robust shift towards a detrimental Th2 response. Our findings suggest a decision tree by moDCs in response to A. fumigatus viable conidia that is absent in Nlrx1-/- moDCs.

2023-01-20 | GSE143964 | GEO

RNA-Seq analysis of gene expression changes by wildtype and Nlrx1 deficient BEAS-2B airway epithelial cells in response to A. fumigatus viable conidia

Project description:RNA-Seq analysis of gene expression changes by wildtype and Nlrx1 deficient BEAS-2B airway epithelial cells in response to A. fumigatus viable conidia

| PRJNA604500 | ENA

Expression analysis of trichostatin A-treated Aspergillus fumigatus Af293

Project description:Investigation of whole genome gene expression level changes in trichostatin A (TSA)-treated A. fumigatus Af293 compared to non-treated A. fumigatus Af293.

2010-06-30 | GSE19682 | GEO

Gene array Airway Smooth Muscle Control vs CoCulture with BEAS2B cells

Project description:Human airway smooth muscle cells were co-cultured with BEAS-2B epithelial cells (or Control). Airway smooth muscle RNA was extracted and sent for Illumina HT-12 micro-array to examine gene expression.

2020-04-30 | E-MTAB-9004 | biostudies-arrayexpress

Expression analysis of trichostatin A-treated Aspergillus fumigatus Af293

Project description:Investigation of whole genome gene expression level changes in trichostatin A (TSA)-treated A. fumigatus Af293 compared to non-treated A. fumigatus Af293. Species: Aspergillus fumigatus; Strain: Af293; Type of array: Eukaryotic Expression (4plex, 2plex for a TSA-treated sample and 2plex for a non-treated sample); Technical replicates: Two per treatment.

2010-06-30 | E-GEOD-19682 | biostudies-arrayexpress

RNA-seq to investigate effect miRNA 210 knockdown of airway respiratory muscle cells treated with BEAS-2B cell condition media

Project description:Airway smooth muscle cells were stimulated with conditioned medium from BEAS-2B cells in the absence (Control) or Inhibition of miR-210.

2020-06-18 | E-MTAB-9224 | biostudies-arrayexpress

Analysis of glucocorticoid receptor (NR3C1), NFkb (p65 subunit), and RNA polymerase 2 (RNAP2) binding in Beas-2B airway epithelial cells

Project description:The objective of this study was to determine binding patterns for GR, 65 and RNAP2 in Beas-2B airway epithelial cells after treatment with dexamethasone (100 nm), TNF (20 ng/ml) or both for one hour. This study utilized duplicate samples for each treatment condition and immunoprecipitation except for p65 immunoprcipitation of TNF treated samples, which was analyzed as a single sample. Input from vehicle treated cells was used a control. Experimental comparisons were made between the following samples/ treatment conditions. Duplicate samples of Beas-2B cells treated with ethanol (vehicle) were used for ChIP of GR, p65, and RNAP2 (2 samples each antibody). Duplicate samples of Beas-2B cells treated with dexamethasone were used for ChIP of GR and RNAP2 (2 samples each antibody). Duplicate samples of Beas-2B cells treated with TNF were used for ChIP of p65 and RNAP2 (1 sample p65, 2 samples RNAP2). Duplicate samples of Beas-2B cells treated with dexamethasone + TNF were used for ChIP of GR, p65 and RNAP2 (2 samples each antibody).

2016-04-01 | E-GEOD-79803 | biostudies-arrayexpress

Clariom S Microarray Expression Data from 4T1 parental and transduced tumors collected from WT and Nlrx1-/- mice

Project description:The immune signaling protein NLRX1 can be either tumor promoting or tumor suppressing in different models of cancer. We demonstrate that in a mammary tumor model of triple-negative breast cancer, NLRX1 impacts tumor volume and lung metastasis. We used this microarray to understand what genes and pathways are impacted by NLRX1 in murine triple-negative mammary tumors to produce the in vivo phenotypes we observed. Abstract from associated publication: Prior studies have defined multiple, but inconsistent, roles for NLRX1 in regulating cancer-associated biological functions. Here, we explore the role of NLRX1 in the highly-metastatic murine 4T1 mammary tumor model. Using Nlrx1-/- mice engrafted with 4T1 tumors, we demonstrate that NLRX1 functions as a tumor suppressor when expressed in healthy host cells. Specifically, NLRX1 attenuates tumor growth and metastasis through suppressing epithelial-mesenchymal transition, tumor-associated eosinophil recruitment, and the lung metastatic niche. Conversely, we demonstrate that NLRX1 functions as a tumor promoter when expressed in 4T1 tumor cells using gain- and loss-of-function studies. Mechanistically, NLRX1 augments 4T1 aggressiveness through regulating epithelial-mesenchymal transition, cell death, proliferation, migration, ROS levels, and mitochondrial respiration. Together, we provide critical insight into NLRX1 function in breast cancer and establish cellular context as the director of the dichotomous role of NLRX1 in mammary tumor metastasis.

2023-08-01 | GSE216937 | GEO

Global transcriptomic analysis of colons of wild type and NLRX1-/- mice with IBD

Project description:NLRX1 is a mitochondrial-associated NOD-like receptor that modulates antiviral immunity, cellular stress, autophagy, and reactive oxygen species (ROS) production. The role of NLRX1 in inflammatory bowel disease (IBD) remains largely unknown. This study aimed to characterize NLRX1-mediated mechanisms of protection from IBD. We investigated the ability of NLRX1 to modulate global colonic gene expression, gut pathology, inflammation and immunity by using loss-of-function approaches in dextran sodiu sulfate (DSS) and CD4+CD45RBhigh transfer colitis models. Colons, spleens, and mesenteric lymph nodes (MLN) were excised for characterizing immune cell subsets, histological analyses, cytokine, RNA sequencing analyses, and autophagy expression, NF-κB activity, and ROS production. The loss of NLRX1 increased severity of disease and colonic histopathology in both models of IBD. Colons of NLRX1-/- mice had significantly increased epithelial ulceration and leukocyte infiltration mostly in the form of neutrophils, lymphocytes, and macrophages in the DSS model, while recipients of NLRX1-/- CD4+ T cells had increased leukocytic infiltration, proliferation, fibrosis, and crypt abscessation in both colon and ileum. The loss of NLRX1 increased numbers of effector T helper (Th1), Th17, and regulatory T cells (Treg) cells in the colonic mucosa and spleen, increased colonic NF-κB activity, upregulation of IL-17, IFNγ and TNF-α production, and increased ROS production. Global transcriptomic analyses demonstrates that NLRX1 regulates immunity and lipid metabolism pathways. NLRX1 ameliorates intestinal pathology during IBD by acting as an internal thermostat that modulates the balance of effector versus regulatory CD4+ T cell responses, and suppressing colonic NF-κB activity, inflammatory cytokine expression, lipid metabolism gene expression, ROS production and autophagy.

2018-03-07 | GSE68419 | GEO

Analysis of local glucocorticoid receptor occupancy at glucocorticoid-repressed inflammatory enhancers in Beas-2B airway epithelial cells II

Project description:This study combined ChIP-seq using two different GR antibodies and stable GR knockdown in Beas-2B airway epithelial cells to determine whether glucocorticoid-mediated repression of inflammatory enhancers requires local GR occupancy

2019-08-27 | GSE135127 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data