Gene expression changes in the host response between resistant and susceptible inbred mouse strains after influenza A infection.
Identifieur interne : 001788 ( Main/Merge ); précédent : 001787; suivant : 001789Gene expression changes in the host response between resistant and susceptible inbred mouse strains after influenza A infection.
Auteurs : Rudi Alberts [Allemagne] ; Barkha Srivastava ; Haiya Wu ; Nuno Viegas ; Robert Geffers ; Frank Klawonn ; Natalia Novoselova ; Tania Zaverucha Do Valle ; Jean-Jacques Panthier ; Klaus SchughartSource :
- Microbes and infection [ 1769-714X ] ; 2010.
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Abstract
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-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.
DOI: 10.1016/j.micinf.2010.01.008
PubMed: 20114087
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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.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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