Unknown,Transcriptomics,Genomics,Proteomics

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Ten day time course of the effect of influenza A infection on spleen gene expression in mice

ABSTRACT: These data were generated as part of a study to model gene regulatory networks influenced by influenza infection. Other tissue compartments included in the study were blood, lung, and lymph node. RNA was extracted from spleens of female mice that did not have any experimental treatment (n = 3, labeled as T-9) or that received intranasal administration of influenza A virus either immediately before (n = 3, T0) or 1 to 10 days before being euthanized for tissue collection (T1 through T10, n =3-4 per day). Gene expression profiles were determined with comprehensive microarrays (Affymetrix Mouse Gene ST 1.0).

ORGANISM(S): Mus musculus

SUBMITTER: Stephen Welle

PROVIDER: E-GEOD-57454 | 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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Ten day time course of the effect of influenza A infection on spleen gene expression in mice

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