Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from well-differentiated human bronchial epithelial cells infected with H1N1 Influenza isolates

ABSTRACT: We used microarrays to compare the gene expression profiles of different H1N1 isolates (seasonal and pandemic) in lung epithelial cells in vitro. Well-differentiated primary human lung, bronchial epithelial cells (wd-NHBE) were infected with two pandemic and one seasaonl H1N1 influenza viruses at a multiplicity of infection of 3.0. The cells were then collected, in triplicate, at 36 hours after infection. This timepoint was selected as we saw significant differences in soluble cytokine and chemokine protein levels at this time point in the supernatant.

ORGANISM(S): Homo sapiens

SUBMITTER: Rachael Gerlach

PROVIDER: E-GEOD-48466 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Background: Pandemic H1N1 influenza A is a newly emerging strain of human influenza that is easily transmitted between people and has spread globally to over 116 countries. Human infection leads to symptoms ranging from mild to severe with lower respiratory complications observed in a small but significant number of infected individuals. Little is currently known about host immunity and Pandemic H1N1 influenza infections. Methods: We examined the pathogenic potential of the pandemic influenza A vaccine strain, A/California/07/2009 (H1N1), in ferrets, and characterized the host immune responses using microarray analysis. Gene expression profiles in lung tissue were compared with those from ferrets infected with A/Brisbane/59/2007. Results: Chemokines CCL2, CCL8, CXCL7 and CXCL10 along with the majority of ISGs were expressed early, correlated to lung pathology, and abruptly decreased expression in 5 days. Interestingly, the drop in innate immune gene expression was replaced by a significant increase in the expression of the adaptive immune genes for granzymes and immunoglobulins. Serum anti-pandemic influenza H1N1 antibodies were also observed on day 7, commensurate with the elimination of viral load. Conclusions: We propose that the innate phase of host immunity causes lung pathology and a delay or failure to effectively switch to the adaptive phase contributes to morbidity and mortality during severe human pandemic H1N1 influenza A infections. Keywords: influenza, immune response, cytokines, chemokines, lung infection, time course In the experiment with influenza A/California/07/2009 (H1N1),15 ferrets were randomly allocated to 5 groups: Day 0 (before infection), and Day 3, 5, 7 and 14 (post infection) with 3 biological replicates for each group. Likewise, a second experiment with A/Brisbane/59/2007 (H1N1) was carried out using the same experimental groups, except for a group in Day 2, instead Day 3. Ferrets were euthanized and lung tissue was excised for RNA purification on the scheduled date. The subsequent gene expression analysis was performed with Affymetrix GeneChip Canine Genome 2.0 Array. Day 0 groups were used as control.

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Expression data from well-differentiated human bronchial epithelial cells infected with H1N1 Influenza isolates

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