
Full text loading...
Category: Bacterial Pathogenesis; Clinical Microbiology
Intracellular Models of Mycobacterium tuberculosis Infection, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555817657/9781555812959_Chap27-1.gif /docserver/preview/fulltext/10.1128/9781555817657/9781555812959_Chap27-2.gifAbstract:
Intracellular models of Mycobacterium tuberculosis infection have proven to be invaluable tools to address diverse questions in mycobacterial research. This chapter begins with an analysis of basic host-pathogen interactions in the infected murine macrophage. It then describes two models in which infected human monocytes interact with lymphocytes and other cells to generate antimycobacterial activity. Lastly, the chapter summarizes clinical trials in which these models were used to analyze the effects of BCG vaccination and other immunologic interventions. The best-studied macrophage antimycobacterial mechanisms are those mediated by (i) the production of nitric oxide (NO) and related reactive nitrogen intermediates (RNI) and (ii) phagolysosomal fusion. Recent microarray analyses have demonstrated that RNI can regulate M. tuberculosis gene expression in vitro. It is becoming clear that M. tuberculosis can interfere with the tethering and fusion machinery involved in phagolysosomal biogenesis. Natural killer (NK) cells have the capacity to kill intracellular M. tuberculosis, whether these cells are isolated from PPD-positive or PPD-negative subjects. The ability of tuberculin reactors to control growth could be blocked by antibodies to gamma interferon (IFN-γ) or tumor necrosis factor (TNF-α) and could be inhibited by methylprednisolone or pentoxifylline. Impaired control of infection was not reconstituted by the addition of exogenous IFN-γ but, in a small cohort, improved following initiation of antiretroviral therapy.
Full text loading...
After phagocytosis, the tubercle bacillus is subject to attack by reactive radicals including various reactive nitrogen intermediates (RNI) and the hydrolytic enzymes of the lysosome. M. tuberculosis has evolved sophisticated means by which these potent antimicrobial activities of macrophages can be evaded.
After phagocytosis, the tubercle bacillus is subject to attack by reactive radicals including various reactive nitrogen intermediates (RNI) and the hydrolytic enzymes of the lysosome. M. tuberculosis has evolved sophisticated means by which these potent antimicrobial activities of macrophages can be evaded.
Immune control of mycobacterial growth in the blood of tuberculosis patients and healthy volunteers a
Immune control of mycobacterial growth in the blood of tuberculosis patients and healthy volunteers a