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Chapter 16 : Infections

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Infections, Page 1 of 2

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Abstract:

The host's cellular immune response appears to determine the fate of the organisms escaping the dormant state. It is the depletion of CD4 cells which leads to the increased rate of reactivation of latent tuberculosis infection in patients dually infected with human immunodeficiency virus (HIV) and tuberculosis. This chapter discusses mechanisms responsible for these phenomena and describes the methods of studying dormancy. Tuberculosis is a chronic infection caused by . predominantly causes disease in the lungs, although it can affect any organ in the body. The infected macrophages spread through the lymphatic channels to regional lymph nodes and then metastasize throughout the body. The interactions of macrophages, lymphocytes, and the organism result in regulation of the immune response in tuberculosis. One study of human alveolar macrophages failed to demonstrate either production of nitric oxide synthase mRNA or nitrous oxide following stimulation of the macrophages by mycobacteria. The human immune response to mycobacteria is decidedly a TH1-like response and is characteristic of the cellular immune response to intracellular pathogens. The adaptive process may then involve a switchover to a reduced metabolic state or to a spore-like state that becomes insusceptible to drug action. Investigation of mycobacterial cells which pass from an actively multiplying state to a low-metabolic nonmultiplying state identified a switch in metabolism to the glyoxalate cycle, which permits adaptation to the usually lethal effects of anaerobiosis.

Citation: Trucksis M. 2000. Infections, p 327-337. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch16

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FIGURE 1

Model of the cellular immune response to tuberculosis. The cellular immune response to tuberculosis infection involves a complex network of bidirectional cellular and cytokine interactions. The dashed arrows and mediators shown in gray represent inhibitory pathways. TNF-α, tumor necrosis factor alpha; MΦ, macrophage; CTL, cytotoxic T lymphocyte.

Citation: Trucksis M. 2000. Infections, p 327-337. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch16
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