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The response of murine primary airway epithelial cells to Influenza infection and the importance of Interferon type I signaling in this response [mAEC].

ABSTRACT: To investigate how murine airway epithelial cells respond to Influenza infection and how important interferon type I signaling is for this response, we harvested airway epithelial cells from the tracheas of wild type, interferon type I knockout(IFNaR-/-) and STAT1 knockout (STAT1-/-) mice and cultured them as previously described (Pickles et al,1998) in polarized airway epithelial cell cultures (mAECs). Triplicate mAECs from each type of mouse (wt,IFNaR-/-,STAT1-/-) were infected with 2X105 PFUs Influenza A (WSN) for 2h or mock inoculated and harvested 24h after infection.

ORGANISM(S): Mus musculus

PROVIDER: GSE32137 | GEO | 2012/03/12

SECONDARY ACCESSION(S): PRJNA154959

REPOSITORIES: GEO

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The response of murine primary airway epithelial cells to Influenza infection and the importance of Interferon type I signaling in this response [mAEC].

Project description:To investigate how murine airway epithelial cells respond to Influenza infection and how important interferon type I signaling is for this response, we harvested airway epithelial cells from the tracheas of wild type, interferon type I knockout(IFNaR-/-) and STAT1 knockout (STAT1-/-) mice and cultured them as previously described (Pickles et al,1998) in polarized airway epithelial cell cultures (mAECs). Triplicate mAECs from each type of mouse (wt,IFNaR-/-,STAT1-/-) were infected with 2X105 PFUs Influenza A (WSN) for 2h or mock inoculated and harvested 24h after infection. Triplicate murine polarized airway epithelial cell cultures from wild type, IFNaR-/- or STAT1-/- mice were mock treated or infected with 2x10^5 PFUs of Influenza A (WSN) for 2h and harvested 24 h post infection.

2012-03-12 | E-GEOD-32137 | biostudies-arrayexpress

The response of human primary airway epithelial cells to Influenza or RSV infection [hAECs_Illumina]

2012-03-12 | GSE32139 | GEO

The response of human primary airway epithelial cells to Influenza or RSV infection [hAECs_Agilent].

2012-03-12 | GSE32138 | GEO

The response of human primary airway epithelial cells to Influenza or RSV infection [hAECs_Agilent].

Project description:To investigate how human airway epithelial cells respond to Influenza or RSV infection, we harvested airway epithelial cells from the mainstream bronchi of human donors and cultured them as previously described (Pickles et al,1998) in a polarized system that resembles the in vivo mucociliary pseudostratified epithelium. Quadruplicate hAEC cultures were infected with 2X105 PFUs Influenza A (Udorn) or with 1x106 PFUs RSV for 2h or mock inoculated and harvested 24h after Influenza infection and 48h after RSV infection. Quadruplicate polarized airway epithelial cell cultures were mock treated or infected with 2x10^5 PFUs of Influenza A (Udorn) for 2h or infected with 1x10^6 PFUs RSV and harvested 24 h post infection for Influenza or 48h post infection for RSV. Total RNA was harvested and gene expression was studied using Genespring GX v7.3.1.

2012-03-12 | E-GEOD-32138 | biostudies-arrayexpress

The response of human primary airway epithelial cells to Influenza or RSV infection [hAECs_Illumina]

Project description:To investigate how human airway epithelial cells respond to Influenza or RSV infection, we harvested airway epithelial cells from the mainstream bronchi of human donors and cultured them as previously described (Pickles et al,1998) in a polarized system that resembles the in vivo mucociliary pseudostratified epithelium. Quadruplicate hAEC cultures were infected with 2X105 PFUs Influenza A (Udorn) or with 1x106 PFUs RSV for 2h or mock inoculated and harvested 24h after Influenza infection and 48h after RSV infection. Quadruplicate polarized airway epithelial cell cultures were infected with 2x10^5 PFUs of Influenza A (Udorn) for 2h or infected with 1x10^6 PFUs RSV and harvested 24 h post infection for Influenza or 48h post infection for RSV.Duplicate cultures were used as controls for each condition (Two cultures were mock treated mor 2h and harvested after 24h for the Influenza infection and 2 cultures were mock treated for 2h and harvested after 48 hours for the RSV infection.Total RNA was harvested and gene expression was studied using Genespring GX v7.3.1.

2012-03-12 | E-GEOD-32139 | biostudies-arrayexpress

The response of PBMCs and primary airway epithelial cells to Influenza and RSV virus

Project description:This SuperSeries is composed of the following subset Series: GSE32137: The response of murine primary airway epithelial cells to Influenza infection and the importance of Interferon type I signaling in this response [mAEC]. GSE32138: The response of human primary airway epithelial cells to Influenza or RSV infection [hAECs_Agilent]. GSE32139: The response of human primary airway epithelial cells to Influenza or RSV infection [hAECs_Illumina] GSE34205: Transcriptional profile of PBMCs in patients with acute RSV or Influenza infection Refer to individual Series

2012-03-12 | E-GEOD-32140 | biostudies-arrayexpress

Quantitative proteomics of airway epithelial cells from COPD and control pre- and post-influenza virus infection

Project description:Chronic obstructive pulmonary disease (COPD) collectively refers to chronic and progressive lung diseases causing not fully reversible limitations in airflow. COPD patients are at high risk for severe respiratory symptoms upon influenza virus infection. Airway epithelial cells provide the first-line antiviral defense, but whether their susceptibility and response to influenza virus infection changes in COPD has not been elucidated. Therefore, this study aimed to i) compare the susceptibility of COPD- and control-derived airway epithelium to influenza virus, and ii) assess protein changes during influenza virus infection by quantitative proteomics. Fluorescent stainings confirmed expression of human- and avian-type influenza virus receptors in primary human bronchial epithelial cells (phBECs) from COPD patients (n=4) and controls (n=3) differentiated at the air-liquid interface. Subjects were closely matched in age, sex, and smoking history and, for COPD-derived phBECs, included stage II (n=2), stage III (n=1) and stage IV (n=1). Proteomics of fully differentiated phBECs pre- and post-influenza A virus infection with A/Puerto Rico/8/34 (PR8) revealed no significant differences between GOLD stage II/ III COPD (n=3) and control phBECs in terms of flu receptor expression, cell type composition, virus replication, or protein profile pre- and post-infection. In contrast, COPD GOLD stage IV phBECs (n=1) showed a distinct pattern of flu receptor expression and a typical COPD phenotype as assessed by a literature-derived panel of 20 proteins and quantification of cell type composition. Independent of health state, proteomics showed a robust antiviral response to influenza virus infection, as well as upregulation of several novel influenza virus-regulated proteins.

2022-12-29 | PXD031461 | Pride

A tracheal aspirate-derived airway basal cell model reveals a proinflammatory epithelial defect in congenital diaphragmatic hernia (ATAC-Seq)

Project description:Congenital diaphragmatic hernia (CDH) is characterized by incomplete closure of the diaphragm and lung hypoplasia. The pathophysiology of lung defects in CDH is poorly understood. To establish a translational model of human airway epithelium in CDH for pathogenic investigation and therapeutic testing, we developed a robust methodology of epithelial progenitor derivation from tracheal aspirates of newborns. Basal stem cells from CDH patients and preterm and term, non-CDH controls were derived and analyzed by bulk RNA-sequencing, ATAC-sequencing, and air-liquid-interface differentiation. Transcriptomic and epigenetic profiling of CDH and non-CDH basal stem cells reveals a disease-specific, proinflammatory signature independent of severity or hernia size. In addition, CDH basal stem cells exhibit defective epithelial differentiation in vitro that recapitulates epithelial phenotypes found in fetal human CDH lung samples and fetal tracheas of the nitrofen rat model of CDH. Furthermore, steroid treatment normalizes epithelial differentiation phenotypes of human CDH basal stem cells in vitro and in nitrofen rat tracheas in vivo. Our findings have identified an interplay between a proinflammatory signature and BSC differentiation as a potential therapeutic target for airway epithelial defects in CDH.

2023-06-30 | GSE211788 | GEO

A tracheal aspirate-derived airway basal cell model reveals a proinflammatory epithelial defect in congenital diaphragmatic hernia (RNA-Seq)

2023-06-30 | GSE211789 | GEO

Analysis of transcriptional differences between ZIKV-infected Ifnar-/- and Ifnar+/- placentas

Project description:Purpose: While type I interferons (IFN) are important for control of viral replication, we see that, upon infection of Ifnar-/- females were crossed to Ifnar+/- males with ZIKV, only Ifnar+/- fetuses are resorbed or develop severe growth restriction. To identify how IFN may be altering placenta development, we performed RNAsequencing on infected and uninfected Ifnar-/- and Ifnar+/- placentas. Methods: Ifnar-/- females were crossed to Ifnar+/- males and infected intravaginally with Cambodian ZIKV at E5.5. Placentas were harvested from infected and uninfected pregnant dams at E10.5. Results/ Conclusions: Comparison of ZIKV-infected Ifnar-/- and Ifnar+/- shows an elevated interferon stimulated gene (ISG) signature in Ifnar+/- placentas but does not reveal any underlying developmental defects that may be causing defects in placenta development.

2017-12-31 | GSE98423 | GEO

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