T-Cells, Stress Proteins, and Pathogenesis of Mycobacterial Infections
When a microbial pathogen meets a mammalian organism, different kinds of relationship may evolve. Exotoxin-producing pathogens can harm the host in a dramatic way without becoming too involved themselves. Purulent bacteria colonize extracellular niches from which they can cause acute-type diseases. In both cases, humoral immunity has a profound effect, and normally either type of pathogen is rapidly eliminated once it is taken up by professional phagocytes. So-called intracellular pathogens establish a lifestyle inside host cells, and many of them survive within macrophages at least for some time. Bacteria of this group include Mycobacterium tuberculosis, M. bovis, M. leprae, Salmonella typhi, Legionella pneumophila, and Listeria monocytogenes—the etiologic agents of tuberculosis, leprosy, typhoid fever, Legionnaire’s disease, and listeriosis, respectively. Although macrophages provide a major habitat for these microorganisms, other host cells can be affected as well, with M. leprae-infected Schwann’s cell providing a notable example.
KeywordsStress Protein Heat Shock Response Mycobacterial Infection Shared Epitope Reactive Oxygen Metabolite
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