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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Evidence for a Crucial Role of a Host Non-coding RNA in Influenza A Virus Replication

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: Carla Winterling

PROVIDER: E-GEOD-45399 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Evidence for a crucial role of a host non-coding RNA in influenza A virus replication.

Winterling Carla C Koch Manuel M Koeppel Max M Garcia-Alcalde Fernando F Karlas Alexander A Meyer Thomas F TF

RNA biology 20131220 1

A growing body of evidence suggests the non-protein coding human genome is of vital importance for human cell function. Besides small RNAs, the diverse class of long non-coding RNAs (lncRNAs) recently came into focus. However, their relevance for infection, a major evolutionary driving force, remains elusive. Using two commercially available microarray systems, namely NCode™ and Sureprint™ G3, we identified differential expression of 42 ncRNAs during influenza A virus (IAV) infection in human lu ...[more]

PMID: 24440876

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NcRNA profiling after Influenza A/WSN/33 infection I

Project description:A growing body of evidence suggests gene regulatory functions for the majority of non-protein-coding RNAs (ncRNAs). Besides small RNAs (sRNAs), the diverse class of long ncRNAs (lncRNAs) recently came into focus of research. So far, the relevance of lncRNAs in infection processes remains elusive. Here, we report the differential expression of several classes of lncRNAs during influenza A virus (IAV) infection in human lung epithelial cells. 2 biological replicates of each condition were hybridzed in an independent color-swap; A549 cells were washed with PBS and then infected with viruses at MOI 1 in infection buffer for for 60M-bM-^@M-^Imin at room temperature. Cells were incubated for the indicated time periods at 37M-bM-^@M-^IM-BM-0C in DMEM supplemented with 0.2% bovine serum albumin, 4M-bM-^@M-^ImM l-glutamine and antibiotics. Supernatants of A/WSN/33 (H1N1) virus infected A549 cells (MOI 5, 4hpi) were exposed to UV light for 5 min and then used to stimulate A549 cells for 4 h Supernatants of A/WSN/33 (H1N1) virus infected A549 cells (MOI 5, 8hpi) were exposed to UV light for 5 min and then used to stimulate A549 cells for 8 h

2014-01-29 | E-GEOD-45397 | biostudies-arrayexpress

NcRNA profiling after Influenza A/WSN/33 infection II

Project description:8h and 24h after A/WSN/33 infection (MOI 1) ncRNA profiling was performed A growing body of evidence suggests gene regulatory functions for the majority of non-protein-coding RNAs (ncRNAs). Besides small RNAs (sRNAs), the diverse class of long ncRNAs (lncRNAs) recently came into focus of research. So far, the relevance of lncRNAs in infection processes remains elusive. Here, we report the differential expression of several classes of lncRNAs during influenza A virus (IAV) infection in human lung epithelial cells. 2 biological replicates of 8h and 24h infection were hybridzed in an independent color-swap

2014-01-29 | E-GEOD-45398 | biostudies-arrayexpress

MicroRNA miR-223 constrains lethal inflammation during Mycobacterium tuberculosis infection

Project description:The molecular mechanisms that control innate cell recruitment during chronic infection and inflammation, such as tuberculosis (TB), are incompletely understood. During TB, myeloid cells infiltrate the lung and sustain local inflammation. We identified microRNA (miR)-223 as one of the most abundant noncoding RNAs in lung parenchyma of TB patients and susceptible mice. MiR-223 controlled lung recruitment of myeloid cells, and consequently, neutrophil-driven lethal inflammation, by directly targeting the chemoattractants CXCL2, CCL3 and IL-6. Our study reveals an essential role for a single miR in TB. Moreover, we identify new targets for and assign novel biological functions to miR-223. By regulating leukocyte chemotaxis via chemoattractants, miR223 is critical for control of TB and probably other nonresolving inflammatory diseases. MicroRNAs expression analysis in whole blood from 8 TB and 8 TST+ subjects. The samples were collected at Makerere University in Kampala, Uganda. Gene expression analysis of whole blood and lung tissue of C57/BL6 and miR-223-/- mouse strains (8-12 weeks of age) after Mtb aerosol infection. Samples were collected at 7, 14 and 21 days post infection.

2014-04-21 | E-GEOD-39163 | biostudies-arrayexpress

Macrophages recognize the Helicobacter pylori type IV secretion system in the absence of TLR signaling

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2015-09-01 | E-GEOD-56791 | biostudies-arrayexpress

Platelets direct monocytes differentiation into multinucleated giant foam cells with suppressive response to mycobacterial stimulus

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2014-01-01 | E-GEOD-45960 | biostudies-arrayexpress

Aryl hydrocarbon receptor senses bacterial pigmented virulence factors and orchestrates anti-bacterial defenses (part 2)

Project description:The aryl hydrocarbon receptor (AhR) is a highly conserved ligand-dependent transcription factor that senses environmental toxins and endogenous ligands, thereby inducing detoxifying enzymes and modulating immune cell differentiation and responses. We hypothesized that AhR not only evolved to sense pollutants from the environment, but also insults of microbial origin. We demonstrate that bacterial pigmented virulence factors, namely the phenazines pyocyanin and 1-hydroxyphenazine from Pseudomonas aeruginosa and the naphthoquinone phthiocol from Mycobacterium tuberculosis, are ligands of AhR. AhR activation leads to degradation of these virulence factors and regulated cytokine and chemokine production. The relevance of AhR to host defense is underlined by heightened susceptibility of AhR-deficient mice, both to P. aeruginosa and M. tuberculosis. Our data demonstrate that AhR senses distinct bacterial virulence factors and controls anti-bacterial responses. We provide evidence for a previously unidentified role for AhR as an intracellular pattern recognition receptor, and identify bacterial pigmented virulence factors as a new class of pathogen-associated molecular patterns. Microarray experiments were performed as dual-color hybridizations. To compensate for dye-specific effects, a dye-reversal color-swap was applied. Quality control and quantification of total RNA amount was assessed using an Agilent 2100 Bioanalyzer (Agilent Technologies) and a NanoDrop 1000 spectrophotometer (Kisker).

2014-01-01 | E-GEOD-48132 | biostudies-arrayexpress

Aryl hydrocarbon receptor senses bacterial pigmented virulence factors and orchestrates anti-bacterial defenses

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-01-01 | E-GEOD-48133 | biostudies-arrayexpress

C646, a Novel p300/CREB-Binding Protein-Specific Inhibitor of Histone Acetyltransferase, Attenuates Influenza A Virus Infection

Project description:Whole-genome data was developed from influenza virus infected A549 cells to better characterize the effect of C646 on influenza virus infection A549 cells were treated with C646 or DMSO for 10 h, and then were infected with A/WSN/33 virus (WSN; H1N1) at a multiplicity of infection (MOI) 2. A549 cells for microarray studies were collected at different times. The gene expression in A549 cells was compared between C646-treated group and DMSO-treated group.

2016-01-07 | E-GEOD-72503 | biostudies-arrayexpress

Pharmacologic inhibition of histone demethylation as a therapy for pediatric brainstem glioma

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-07-16 | E-GEOD-59497 | biostudies-arrayexpress

Type I IFN signaling promotes local inflammation in pulmonary tuberculosis

Project description:The critical role of type I IFN (IFN I ) in viral disease is thoroughly documented while their function in bacterial infection remains ambiguous. General interest in biological functions of IFN I in Mycobacterium tuberculosis (Mtb) infection was raised by the identification of a distinct IFN I gene expression signature in tuberculosis (TB) patients. Here we demonstrate that TB-susceptible mice lacking the receptor for IFN I (IFNAR1) were protected from death upon aerogenic infection with Mtb. Increased survival was accompanied by reduced bacterial burden and ameliorated lung pathology as well as diminished production of proinflammatory IL-1?, among other cytokines. IFNAR1 signaling did not affect T cell responses, but markedly altered migration of inflammatory monocytes and neutrophils to the lung during pulmonary TB. This process was orchestrated by presence of IFNAR1 in both immune and tissue-resident radioresistant cells. IFNAR1-driven TB susceptibility was initiated by CXCL5/CXCL1-driven accumulation of neutrophils into alveoli and subsequently a distinct compartmentalization of Mtb in lung phagocytes. We conclude that IFN I alters early innate events at the site of Mtb invasion leading to unleashed inflammation. Hence, our data furnish a mechanistic explanation for the detrimental role of IFN I in pulmonary TB. dual-color color-swap

2013-12-31 | E-GEOD-44848 | biostudies-arrayexpress

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