title: Crosstalk between Mycobacterium tuberculosis and the host cell.
abstract: The successful establishment and maintenance of a bacterial infection depend on the pathogen's ability to subvert the host cell's defense response and successfully survive, proliferate, or persist within the infected cell. To circumvent host defense systems, bacterial pathogens produce a variety of virulence factors that potentiate bacterial adherence and invasion and usurp host cell signaling cascades that regulate intracellular microbial survival and trafficking. Mycobacterium tuberculosis, probably one of the most successful pathogens on earth, has coexisted with humanity for centuries, and this intimate and persistent connection between these two organisms suggests that the pathogen has evolved extensive mechanisms to evade the human immune system at multiple levels. While some of these mechanisms are mediated by factors released by M. tuberculosis, others rely on host components that are hijacked to prevent the generation of an effective immune response thus benefiting the survival of M. tuberculosis within the host cell. Here, we describe several of these mechanisms, with an emphasis on the cyclic nucleotide signaling and subversion of host responses that occur at the intracellular level when tubercle bacilli encounter macrophages, a cell that becomes a safe-house for M. tuberculosis although it is specialized to kill most microbes.
authors.affiliation: Department of Medicine, Johns Hopkins University, School of Medicine, Baltimore, MD, USA; Howard Hughes Medical Institute, Chevy Chase, MD, USA.
authors.forename: Bappaditya
authors.initials: B
authors.lastname: Dey
authors.affiliation: Department of Medicine, Johns Hopkins University, School of Medicine, Baltimore, MD, USA; Howard Hughes Medical Institute, Chevy Chase, MD, USA. Electronic address: wbishai@jhmi.edu.
authors.forename: William R
authors.initials: WR
authors.lastname: Bishai
mesh_terms: D001426:Bacterial Proteins / Q000235:genetics / Q000276:immunology; D000242:Cyclic AMP / Q000276:immunology / Q000378:metabolism; D005786:Gene Expression Regulation; D006801:Humans; D057131:Immune Evasion; D007113:Immunity, Innate; D008168:Lung / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D016676:Macrophages, Alveolar / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D009169:Mycobacterium tuberculosis / Q000276:immunology / Q000472:pathogenicity*; D010588:Phagosomes / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D011135:Polysaccharides, Bacterial / Q000096:biosynthesis / Q000276:immunology; D051192:Receptors, Pattern Recognition / Q000235:genetics / Q000276:immunology; D015398:Signal Transduction; D014397:Tuberculosis, Pulmonary / Q000235:genetics / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D014774:Virulence
chemical_list: D001426:Bacterial Proteins; D011135:Polysaccharides, Bacterial; D051192:Receptors, Pattern Recognition; D000242:Cyclic AMP
keywords: Cyclic AMP; Cyclic di-AMP; Immunity; Interferon; Macrophage; Mycobacterium tuberculosis