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

被引:50
作者
Alberts, Rudi [1 ]
Srivastava, Barkha [1 ]
Wu, Haiya [1 ]
Viegas, Nuno [1 ]
Geffers, Robert [2 ]
Klawonn, Frank [3 ]
Novoselova, Natalia [4 ]
do Valle, Tania Zaverucha [5 ]
Panthier, Jean-Jacques [5 ]
Schughart, Klaus [1 ,6 ]
机构
[1] Helmholtz Ctr Infect Res, Dept Infect Genet, D-38124 Braunschweig, Germany
[2] Helmholtz Ctr Infect Res, Dept Cell Biol, D-38124 Braunschweig, Germany
[3] Univ Appl Sci Braunschweig Wolfenbuettel, Dept Comp Sci, D-38302 Wolfenbuettel, Germany
[4] Natl Acad Sci Belarus, United Inst Informat Problems, Minsk 220012, BELARUS
[5] Inst Pasteur, Dept Dev Biol, F-75015 Paris, France
[6] Univ Vet Med Hannover, D-30559 Hannover, Germany
关键词
Inbred mouse strains; Influenza A virus; Gene expression microarray; VIRUS-INFECTION; MICROARRAY ANALYSIS; EPITHELIAL-CELLS; IMMUNE-RESPONSE; H5N1; INFECTION; LUNG; MICE; PATHOGENESIS; CHEMOKINES; PNEUMONIA;
D O I
10.1016/j.micinf.2010.01.008
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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 (C5713L/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 D13A/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 (C) 2010 Elsevier Masson SAS All rights reserved.
引用
收藏
页码:309 / 318
页数:10
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