engleski

Što medicinski biokemičar treba znati o tuberkuloznoj infekciji

Immune response to M. tuberculosis is a classic example of the cell-mediated immunity. After uptake of M. tuberculosis in alveolar macrophages a several scenarios are possible: in healthy subjects M. tuberculosis may be destroyed immediately (in this case no adaptive T-cell response is developed). Mycobacteria which escape this destruction will multiply and macrophages will be disrupted. Inflammatory cells, including blood monocytes are attracted to the lung. Monocytes will differentiate into macrophages and ingest (not destroy) mycobacteria, so mycobacteria may multiply logarithmmically. Within 2 fo 6 weeks, T- cell-mediated immunity develops, i.e. antigen-specific T-lymphocytes arrive, proliferate, and activate macrophages (resulting in granuloma formation) to kill the intracellular mycobacteria. Subsequently, central necrosis inhibits extracellular growth of M. tuberculosis. In 90% of people infection may become dormant, and 10% of people may develop tuberculosis (TB). Protective anti-mycobacterial immunity involves many T-lymphocytes activating the macrophages and their microbicidal functions. Their activation requires the release of numerous cytokines, such as IL-12, IL-10, interferon-gamma (IFN-γ) or tumour necrosis factor alpha (TNF-α). Young children and elderly persons have the highest risk of development TB, since they have relatively weak immune defences, because of immature system (children) or age-related immune disfunction (elderly people). Persons with impaired immunity due to HIV infection or patients who must receive anti-TNF-α medication are at high risk of TB development. Microbiologic techniques (eg. finding of M. tuberculosis in culture) enable detection M. tuberculosis in biological specimens, and biochemical methods (eg. ex vivo determination of IFN-γ) enable detection tuberculosis infection even in latent stage.

tuberculosis infection; laboratory medicine

Sažetak rada objavljen je u časopisu Biochemia Medica