| Literature DB >> 20114087 |
Rudi Alberts1, Barkha Srivastava, Haiya Wu, Nuno Viegas, Robert Geffers, Frank Klawonn, Natalia Novoselova, Tania Zaverucha do Valle, Jean-Jacques Panthier, Klaus Schughart.
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. Copyright 2010 Elsevier Masson SAS. All rights reserved.Entities:
Mesh：
Year: 2010 PMID： 20114087 DOI： 10.1016/j.micinf.2010.01.008
Source DB: PubMed Journal: Microbes Infect ISSN： 1286-4579 Impact factor: 2.700