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Profiling and bioinformatics analysis of hsa-miRNAs involved in A549 strain of human alveolar epithelial type II cell line infected with A/Zhejiang/DTID-ZJU02/2009(H1N1)

ABSTRACT: A/Zhejiang/DTID-ZJU02/2009(H1N1) is a strain of the swine-origin influenza A(H1N1) virus isolated during the human swine flu outbreak of 2009. To analyze the miRNA expression profiles of A549 cells infected with A/Zhejiang/DTID-ZJU02/2009(H1N1) at 0, 24, 48, and 72 h post-infection (hpi) and investigate the relation between the miRNA expression profile and its pathogenesis, Human MicroRNA Array v2.0 was applied. At 24 hpi, 174 miRNAs were detected to change their expression compared with 0 hpi, 28 of them increased and 146 decreased. At 48 hpi, 214 changed miRNAs were detected, 21 of them increased and 193 decreased. At 72 hpi, 282 changed miRNAs were detected, 19 of them increased and 263 decreased. Targets of the 21 significantly differentially expressed miRNAs were analyzed by bioinformatics technology. The function categories of the predicted targets were analyzed by GO(Gene ontology) annotation. The signaling pathways involving the changed miRNAs were analyzed by KEGG(Kyoto Encyclopedia of Genes and Genomes) and GO annotation. Four key signaling pathways were identified, namely, the MAPK, apoptosis, JAK_STAT, and toll-like receptor signaling pathways. The apoptosis and MAPK signaling pathways were activated by all miRNAs, whereas the JAK_STAT and toll-like receptor signaling pathways were activated by some miRNAs but inhibited by the others, suggesting balance in the host–virus interaction. We also constructed and analyzed the protein-protein interaction network of all the predicted targets and found some key nodes. This finding provides a picture of miRNA expression in A549 cells infected with A/Zhejiang/DTID-ZJU02/2009(H1N1) as complete as possible, which may provide important information for investigation of H1N1 pathogenesis and therapeutic method.

ORGANISM(S): Homo sapiens

PROVIDER: GSE52105 | GEO | 2013/11/06

SECONDARY ACCESSION(S): PRJNA226692

REPOSITORIES: GEO

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Project description:A/Zhejiang/DTID-ZJU02/2009(H1N1) is a strain of the swine-origin influenza A(H1N1) virus isolated during the human swine flu outbreak of 2009. To analyze the miRNA expression profiles of A549 cells infected with A/Zhejiang/DTID-ZJU02/2009(H1N1) at 0, 24, 48, and 72 h post-infection (hpi) and investigate the relation between the miRNA expression profile and its pathogenesis, Human MicroRNA Array v2.0 was applied. At 24 hpi, 174 miRNAs were detected to change their expression compared with 0 hpi, 28 of them increased and 146 decreased. At 48 hpi, 214 changed miRNAs were detected, 21 of them increased and 193 decreased. At 72 hpi, 282 changed miRNAs were detected, 19 of them increased and 263 decreased. Targets of the 21 significantly differentially expressed miRNAs were analyzed by bioinformatics technology. The function categories of the predicted targets were analyzed by GO(Gene ontology) annotation. The signaling pathways involving the changed miRNAs were analyzed by KEGG(Kyoto Encyclopedia of Genes and Genomes) and GO annotation. Four key signaling pathways were identified, namely, the MAPK, apoptosis, JAK_STAT, and toll-like receptor signaling pathways. The apoptosis and MAPK signaling pathways were activated by all miRNAs, whereas the JAK_STAT and toll-like receptor signaling pathways were activated by some miRNAs but inhibited by the others, suggesting balance in the host–virus interaction. We also constructed and analyzed the protein-protein interaction network of all the predicted targets and found some key nodes. This finding provides a picture of miRNA expression in A549 cells infected with A/Zhejiang/DTID-ZJU02/2009(H1N1) as complete as possible, which may provide important information for investigation of H1N1 pathogenesis and therapeutic method. the miRNA expression profiles of A549 cells infected with A/Zhejiang/DTID-ZJU02/2009(H1N1) at 0, 24, 48, and 72 h post-infection (hpi) were analyzed and the relation between the miRNA expression profile and its pathogenesis was investigated.

Project description:Background: The 2009 pandemic H1N1 influenza virus emerged in swine and quickly became a major global health threat. In mouse, non-human primate, and swine infection models, the pH1N1 virus efficiently replicates in the lung and induces pro-inflammatory host responses; however, whether similar or different cellular pathways were impacted by pH1N1 virus across independent infection models remains to be further defined. To address this, we have performed a comparative transcriptomic analysis of acute host responses to a single pH1N1 influenza virus, A/California/04/2009 (CA04), in the lung of mice, macaques and swine. Results: Despite similarities in the clinical course, we observed differences in inflammatory molecules elicited, and the kinetics of their gene expression changes across all three species. The retinoid X receptor (RXR) signaling pathway controlling pro-inflammatory and metabolic processes was differentially regulated during infection in each species, though the heterodimeric RXR partner, pathway associated signaling molecules, and gene expression patterns differed in each species. Conclusions: By comparing transcriptional changes in the context of clinical and virological measures, we identified differences in the host transcriptional response to pH1N1 virus across independent models of acute infection. Antiviral resistance and the emergence of new influenza viruses have placed more focus on developing drugs that target the immune system. Underlying overt clinical disease are molecular events that suggest therapeutic targets identified in one host may not be appropriate in another. The goal of this experiment was to use global gene expression profiling to understand swine lung host responses to pandemic H1N1 influenza A/Californica/04/2009 (CA04) virus infection and compare acute host responses across independent species. Four-week-old crossbred pigs (Sus Scrofa) were inoculated intratracheally with either 10^6 TCID50/pig egg-derived 2009 pandemic influenza A/California/04/2009 virus (n = 5) or mock inoculated with non-infectious cell culture supernatant (control; n = 4). Animals were euthanized on day 7 post-infection and lung samples were used for microarray.

Project description:Background: The 2009 pandemic H1N1 influenza virus emerged in swine and quickly became a major global health threat. In mouse, non-human primate, and swine infection models, the pH1N1 virus efficiently replicates in the lung and induces pro-inflammatory host responses; however, whether similar or different cellular pathways were impacted by pH1N1 virus across independent infection models remains to be further defined. To address this, we have performed a comparative transcriptomic analysis of acute host responses to a single pH1N1 influenza virus, A/California/04/2009 (CA04), in the lung of mice, macaques and swine. Results: Despite similarities in the clinical course, we observed differences in inflammatory molecules elicited, and the kinetics of their gene expression changes across all three species. The retinoid X receptor (RXR) signaling pathway controlling pro-inflammatory and metabolic processes was differentially regulated during infection in each species, though the heterodimeric RXR partner, pathway associated signaling molecules, and gene expression patterns differed in each species. Conclusions: By comparing transcriptional changes in the context of clinical and virological measures, we identified differences in the host transcriptional response to pH1N1 virus across independent models of acute infection. Antiviral resistance and the emergence of new influenza viruses have placed more focus on developing drugs that target the immune system. Underlying overt clinical disease are molecular events that suggest therapeutic targets identified in one host may not be appropriate in another. The goal of this experiment was to use global gene expression profiling to understand mouse lung cellular responses to pandemic H1N1 influenza A/Californica/04/2009 virus infection. Six-to-eight-week-old female BALB/c mice were anesthetized and inoculated with either 50 Î¼l of phosphate-buffered saline (PBS; Mock) or with 10^6 pfu of pandemic H1N1 influenza A/California/04/2009 virus in a 50 Î¼l volume, and whole lungs were collected at days 1, 3 and 5 post-inoculation. Lung samples from 9 animals for the infection group were used for array analysis, three animals per time point. Lung samples from 8 animals for the mock group were used for array analysis, three animals for the day 1 and 3 time points and 2 animals for the day 5 time point.

Project description:Background: The 2009 pandemic H1N1 influenza virus emerged in swine and quickly became a major global health threat. In mouse, non-human primate, and swine infection models, the pH1N1 virus efficiently replicates in the lung and induces pro-inflammatory host responses; however, whether similar or different cellular pathways were impacted by pH1N1 virus across independent infection models remains to be further defined. To address this, we have performed a comparative transcriptomic analysis of acute host responses to a single pH1N1 influenza virus, A/California/04/2009 (CA04), in the lung of mice, macaques and swine. Results: Despite similarities in the clinical course, we observed differences in inflammatory molecules elicited, and the kinetics of their gene expression changes across all three species. The retinoid X receptor (RXR) signaling pathway controlling pro-inflammatory and metabolic processes was differentially regulated during infection in each species, though the heterodimeric RXR partner, pathway associated signaling molecules, and gene expression patterns differed in each species. Conclusions: By comparing transcriptional changes in the context of clinical and virological measures, we identified differences in the host transcriptional response to pH1N1 virus across independent models of acute infection. Antiviral resistance and the emergence of new influenza viruses have placed more focus on developing drugs that target the immune system. Underlying overt clinical disease are molecular events that suggest therapeutic targets identified in one host may not be appropriate in another. The goal of this experiment was to use global gene expression profiling to understand non-human primate lung cellular responses to pandemic H1N1 influenza A/California/04/2009 virus infection. Four-to-fifteen-year-old cynomologous macaques were infected with CA04 virus (n = 4) under anesthesia through a combination of intratracheal (4 ml), intranasal (0.5 ml per nostril), conjunctival (0.5 ml per eyelid) and oral (1 ml) routes with a suspension containing 10^6 TCID50/ml (total infectious dose was 7x10^6 TCID50). Animals were euthanized on 1 and 6 days post-inoculation (n = 2 per time point), and total RNA was extracted from lung samples and analyzed by microarray. Pooled RNA from lungs of uninfected animals served as the reference.

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Profiling and bioinformatics analysis of hsa-miRNAs involved in A549 strain of human alveolar epithelial type II cell line infected with A/Zhejiang/DTID-ZJU02/2009(H1N1)

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