Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Time series of flu-infected lungs of DBA/2J and C57BL/6J mice

ABSTRACT: DBA/2J (D2) and C57BL/6J mice (B6) were infected intra-nasally with 2x10^3 FFU of influenza A H1N1 (PR8) virus. Lungs were collected from mock-infected controls or at day 1,2,3,4 post infection. Expression data were obtained from three independent experiments. We infected a highly susceptible mouse strain (D2) and a resistant strain (B6) with PR8 and performed a genome-wide expression analysis. We found genes expressed in lung epithelium that were specifically down-regulated in D2 mice, whereas a cluster of genes on chromosome 3 was only down-regulated in B6. In both mouse strains, chemokines, cytokines and interferon-response genes were up-regulated, indicating that the main innate immune defense pathways were activated. However, many immune response genes were up-regulated in D2 much stronger than in B6, and several immune response genes were exclusively regulated in D2. Thus, susceptible D2 mice showed a hyper-inflammatory response. This response is similar to infections with highly pathogenic influenza virus and may serve as a paradigm for a hyper-inflammatory host response to influenza A virus.

ORGANISM(S): Mus musculus

SUBMITTER: Claudia Pommerenke 

PROVIDER: E-MTAB-835 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression changes in the host response between resistant and susceptible inbred mouse strains after influenza A infection.

Alberts Rudi R   Srivastava Barkha B   Wu Haiya H   Viegas Nuno N   Geffers Robert R   Klawonn Frank F   Novoselova Natalia N   do Valle Tania Zaverucha TZ   Panthier Jean-Jacques JJ   Schughart Klaus K  

Microbes and infection 20100128 4

Inbred mouse strains exhibit differences in susceptibility to influenza A infections. However, the molecular mechanisms underlying these differences are unknown. Therefore, we infected a highly susceptible mouse strain (DBA/2J) and a resistant strain (C57BL/6J) with influenza A H1N1 (PR8) and performed genome-wide expression analysis. We found genes expressed in lung epithelium that were specifically down-regulated in DBA/2J mice, whereas a cluster of genes on chromosome 3 was only down-regulate  ...[more]

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