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Crosstalk between Mycobacterium tuberculosis and the host cell.
Bappaditya Dey1, William R Bishai1
1Department of Medicine, Johns Hopkins University, School of Medicine, Baltimore, MD, USA; Howard Hughes Medical Institute, Chevy Chase, MD, USA.
Seminars in Immunology
|October 12, 2014
Summary
Mycobacterium tuberculosis evades host defenses by hijacking cellular processes. This pathogen manipulates cyclic nucleotide signaling within macrophages, its preferred intracellular niche, to ensure survival.
Area of Science:
- Microbiology
- Immunology
- Cell Biology
Background:
- Bacterial pathogens must overcome host defenses for successful infection.
- Mycobacterium tuberculosis (M. tuberculosis) has evolved complex mechanisms to evade the human immune system.
- Intracellular survival and proliferation are key to M. tuberculosis pathogenesis.
Purpose of the Study:
- To describe M. tuberculosis mechanisms for subverting host cell defenses.
- To emphasize the role of cyclic nucleotide signaling in intracellular survival.
- To elucidate how M. tuberculosis manipulates macrophage functions.
Main Methods:
- Review of known virulence factors and host-pathogen interactions.
- Focus on intracellular events following M. tuberculosis-macrophage encounter.
- Analysis of host cell signaling pathways subverted by M. tuberculosis.
Main Results:
- M. tuberculosis utilizes both secreted factors and hijacked host components to evade immunity.
- Cyclic nucleotide signaling plays a crucial role in intracellular survival.
- Macrophages, specialized for microbial killing, become a niche for M. tuberculosis.
Conclusions:
- M. tuberculosis employs sophisticated strategies to persist within host cells.
- Subversion of host cell signaling, particularly cyclic nucleotides, is critical for pathogenesis.
- Understanding these mechanisms offers insights into host-pathogen interactions and potential therapeutic targets.
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