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dc.contributor.authorAlberts, Rudi
dc.contributor.authorSrivastava, Barkha
dc.contributor.authorWu, Haiya
dc.contributor.authorViegas, Nuno
dc.contributor.authorGeffers, Robert
dc.contributor.authorKlawonn, Frank
dc.contributor.authorNovoselova, Natalia
dc.contributor.authordo Valle, Tania Zaverucha
dc.contributor.authorPanthier, Jean-Jacques
dc.contributor.authorSchughart, Klaus
dc.date.accessioned2010-04-12T09:25:07Zen
dc.date.available2010-04-12T09:25:07Zen
dc.date.issued2010-04en
dc.identifier.citationGene expression changes in the host response between resistant and susceptible inbred mouse strains after influenza A infection. 2010, 12 (4):309-18 Microbes Infect.en
dc.identifier.issn1769-714Xen
dc.identifier.pmid20114087en
dc.identifier.doi10.1016/j.micinf.2010.01.008en
dc.identifier.urihttp://hdl.handle.net/10033/96275en
dc.description.abstractInbred 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-regulated in C57BL/6J. 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 DBA/2J much stronger than in C57BL/6J, and several immune response genes were exclusively regulated in DBA/2J. Thus, susceptible DBA/2J 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.
dc.language.isoenen
dc.titleGene expression changes in the host response between resistant and susceptible inbred mouse strains after influenza A infection.en
dc.typeArticleen
dc.contributor.departmentDepartment of Infection Genetics, Helmholtz Centre for Infection Research, Braunschweig, Germany.en
dc.identifier.journalMicrobes and infection / Institut Pasteuren
refterms.dateFOA2018-06-13T15:58:38Z
html.description.abstractInbred 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-regulated in C57BL/6J. 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 DBA/2J much stronger than in C57BL/6J, and several immune response genes were exclusively regulated in DBA/2J. Thus, susceptible DBA/2J 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.


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