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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. 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.

ORGANISM(S): Mus musculus

SUBMITTER: IOANNIS IOANNIDIS

PROVIDER: E-GEOD-32137 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

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.

2012-03-12 | GSE32137 | 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

Novel non-canonical role of STAT1 in Natural Killer cell cytotoxicity

Project description:STAT1 is an important regulator of NK cell maturation and cytotoxicity. Although the consequences of Stat1-deficiency have been described in detail the underlying molecular functions of STAT1 in NK cells are only partially understood. Here we describe a novel non-canonical role of STAT1 that was unmasked in NK cells expressing Stat1-Y701F. This mutation prevents JAK-dependent phosphorylation, subsequent nuclear translocation and cytokine-induced transcriptional activity. As expected Stat1-Y701F mice displayed impaired NK cell maturation comparable to Stat1-/- animals. In contrast Stat1-Y701F NK cells exerted a significantly enhanced cytotoxicity in vitro and in vivo suggesting a so-far unknown cytoplasmic function. Using immunofluorescence technology we uncovered the recruitment of STAT1 to the immunological synapse during NK cell killing. A Stat1ind mouse expressing FLAG-tagged STAT1α was used to study the STAT1α interactome in NK cells. Mass spectrometry revealed that STAT1 directly binds proteins involved in cell junction formation and proteins associated to membrane or membrane-bound vesicles. We propose a novel function for STAT1 in the immunological synapse of NK cells regulating tumor surveillance and cytotoxicity.

2016-10-07 | PXD002206 | Pride

RNA-seq of whole lungs from Irgm1-/- and wildtype littermates mice that were either uninfected or infected with influenza for 3, 6, or 10 days

Project description:We found that a dose of influenza (5,000 pfu of recombinant influenza A/WSN/33 (rWSN) H1N1 virus strain) that resulted in 50% mortality in wildtype littermate control mice showed minimal mortality in Irgm1-/- mice, indicating that Irgm1 deficiency was protective during influenza infection. This protective effect was dependent on the Type I interferon receptor Ifnar. We performed transcriptional profiling to identify molecular mechanisms associated with protection from influenza infection in Irgm1-/- lung. Both male and female mice were used at 8-12 weeks of age. Lung gene expression was assessed by RNA-seq at the following times post-influenza infection: Day 3 (early time point, early histological damage present in control mice), Day 6 (intermediate time point, late histological damage present in control mice) and Day 10 (late time point, morbidity and mortality present in control mice).

2017-08-08 | E-MTAB-5337 | biostudies-arrayexpress

Gene expression profile associated with loss of IFNAR signaling or loss of LTβR singlaing in spleen marginal zone macrophages (MZM) in autoimmune BXD2 mice

Project description:Loss of the interactions between lymphotoxin and its receptor was associated with MZM apoptotic cell clearance defects in BXD2 mice whereas loss of IFNAR in BXD2 mice normalized the function of MZMs. The analysis also intended to use MZMs isolated from BXD2-Ifnar-/- mice and BXD2 mice treated with sLTbR-Fc to identify the common pathways regulating the MZM function in these mice. Samples were derived from MZMs of the spleen of BXD2 mice which exhibit spontaneous defects in MZMs, BXD2-Ifnar-/- mice which exhibit normalized MZMs, and BXD2 mice administered sLTβR-Fc which exhibit further defects in MZMs

2015-04-01 | E-GEOD-66687 | biostudies-arrayexpress

Genome-wide analysis of gene expression in human macrophages in response to infection with influenza A viruses expressing full length or truncated non-structural protein NS1.

Project description:Analysis of gene expression in human macrophages infected with influenza A viruses expressing full length or truncated NS1 protein. The hypothesis tested was that C-terminal truncations of viral NS1 protein attenuate the capability of NS1 to limit activation of host antiviral and immune response genes. Cells were infected with influenza A/WSN/33 viruses expressing wild type NS1 protein (WSN-230), NS1 protein of 220 aa long (WSN-220) and NS1 protein of 202 aa long (WSN-202) on non-infected (Mock)

2014-10-08 | GSE62127 | GEO

in vitro kinase assays Identified of STAT1 phosphorylation sites-mediated LATS2

Project description:LATS1/2 are frequently down-regulated or mutated in endometrial cancer (EC), yet their exact role in endometrial tumor progression remains unclear. In this study, we unexpectedly discovered a new function of LATS1/2 in regulating MHC class I expression in EC. Knockout of LATS1/2 in EC cells led to significant down-regulation of multiple genes within the MHC/HLA Class I family, which weakened the killing effects of PBMCs on tumor cells. Importantly, we found that the regulation of MHC/HLA expression by LATS1/2 does not depend on the classical Hippo pathway but rather involves their direct interaction with STAT1. This interaction causes STAT1 to be phosphorylated at Ser727 or Ser532, promoting its accumulation and movement into the nucleus and enhancing the transcriptional activation of IRF1/NLRC5 on MHC-I. Additionally, we demonstrated that the kinase-dead mutant LATS1/2 weakens STAT1 phosphorylation at Ser727, supporting our findings. Our results show a positive correlation between the expression levels of LATS1/2, MHC-I, CD8, and p-STAT1 in tissue samples of EC, providing further evidence to support our discoveries. Overall, our findings reveal novel molecular mechanisms underlying tumor immunogenicity deficiency and suggest that LATS1/2 may serve as an immunotherapy biomarker for targeting EC.

2024-06-16 | PXD043500 | Pride

ATF3 is a novel regulator of mouse neutrophil migration.

Project description:Expression of the activating transcription factor 3 (ATF3) gene is induced by Toll-like receptor (TLR) signaling. In turn, ATF3 protein inhibits the expression of various TLR-driven pro-inflammatory genes. Given its counter-regulatory role in diverse innate immune responses, we defined the effects of ATF3 on neutrophilic airway inflammation in mice. ATF3 deletion was associated with increased lipopolysaccharide (LPS)-driven airway epithelia production of CXCL1, but not CXCL2, findings concordant with a consensus ATF3-binding site identified solely in the Cxcl1 promoter. Unexpectedly, ATF3-deficient mice did not exhibit increased airway neutrophilia after LPS challenge. Bone marrow chimeras revealed a specific reduction in ATF3-/- neutrophil recruitment to wild type lungs. In vitro, ATF3-/- neutrophils exhibited a profound chemotaxis defect. Global gene expression analysis identified ablated Tiam2 expression in ATF3-/- neutrophils. TIAM2 regulates cellular motility by activating Rac1-mediated focal adhesion disassembly. Notably, ATF3-/- and ATF3-sufficient TIAM2 knockdown neutrophils, both lacking TIAM2, exhibited increased focal complex area, along with excessive CD11b-mediated F-actin polymerization. Together, our data describe a dichotomous role for ATF3-mediated regulation of neutrophilic responses: inhibition of neutrophil chemokine production, but promotion of neutrophil chemotaxis. Ly6G+ neutrophils were purified by magnetic beads from WT or ATF3 KO bone marrow and RNA was immediately isolated for global gene expression using microarrays.

2014-04-05 | E-GEOD-53973 | biostudies-arrayexpress

STAT1 transcription factor in Human HeLa S3

Project description:We report the results of chromatin immunoprecipitation following by high-thoughput tag sequencing (ChIP-Seq) using the GA II platform from Illumina for the human transcription factor STAT1 in HeLa S3 cells. The STAT1 ChIP was performed using HeLa S3 cells that are stimulated using gamma-interferon. We have also generated a seqenced input DNA dataset for gamma-interferon stimulated HeLa S3 cells. Raw data for this study is available for download from the Short Read Archive database at: http://www.ncbi.nlm.nih.gov/Traces/sra/sra.cgi?study=SRP000703. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Examination of the STAT1 transcription factor in Human HeLa S3.

2008-09-15 | E-GEOD-12782 | biostudies-arrayexpress

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