Expression profiling of host pathogen interactions:: How Mycobacterium tuberculosis and the macrophage adapt to one another

被引:40
作者
Schnappinger, Dirk [1 ]
Schoolnik, Gary K.
Ehrt, Sabine
机构
[1] Cornell Univ, Weill Med Coll, Dept Microbiol & Immunol, New York, NY 10021 USA
[2] Stanford Univ, Sch Med, Dept Med, Div Infect Dis & Geog Med, Stanford, CA 94305 USA
[3] Stanford Univ, Sch Med, Dept Microbiol & Immunol, Stanford, CA 94305 USA
[4] Cornell Univ, Weill Grad Sch Med Sci, Grad Program Mol Biol, New York, NY 10021 USA
[5] Cornell Univ, Weill Grad Sch Med Sci, Grad Program Immunol & Microbial Pathogenesis, New York, NY 10021 USA
关键词
microarray gene expression analysis; macrophage activation; innate immunity; tuberculosis; pathogenicity;
D O I
10.1016/j.micinf.2005.10.027
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
It has recently become feasible to quantify all mRNAs encoded by the genomes of bacterial pathogens and their eukaryotic host cells and to apply this approach to study the interaction of Mycobacterium tuberculosis with its primary host cell, the macrophage. These studies helped to identify regulatory circuits which mediate adaptation of the M. tuberculosis transcriptome to intraphagosomal environments and stimulated hypotheses for the function of these circuits in human tuberculosis. The macrophage transcriptome reacts to infections with the induction of a pathogen-unspecific expression program as well as the induction of pathogen-specific expression signatures, both of which contribute to the immunologic activation of the infected cell. M. tuberculosis induced changes in the macrophage transcriptome are mediated by Toll-like receptor dependent and Toll-like receptor independent signal transduction pathways. This response is shaped by macrophage produced reactive nitrogen and oxygen molecules and affected by viability and virulence of the pathogen. (c) 2006 Elsevier SAS. All rights reserved.
引用
收藏
页码:1132 / 1140
页数:9
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