Reduced apoptosis and increased inflammatory cytokines in granulomas caused by tuberculous compared to non-tuberculous mycobacteria: role of MPT64 antigen in apoptosis and immune response.

摘要: Inhibition of apoptosis infected macrophages by pathogenic mycobacteria is suggested to be an important virulence mechanism, but little known about the mycobacterial proteins involved in inhibition apoptosis. In this study we investigated differences and immune response their correlation with expression Mycobacterium tuberculosis complex-specific secretory protein MPT64 lesions caused tuberculous or non-tuberculous analysing situ apoptosis-related (FasL, Fas, Bax, Bcl-2), apoptotic cells, inflammatory cytokines [tumour necrosis factor (TNF)-alpha, interleukin (IL)-10, transforming growth (TGF)-beta, interferon (IFN)-gamma] antigen. The discrimination was made nested polymerase chain reaction (PCR) amplification IS6110, which specific for M. complex organisms. Forty-seven cases lymphadenitis necrotic granulomas were evaluated. With PCR, 30/47 positive tuberculosis. antigen detected specifically PCR-positive cases. Granulomas had fewer higher numbers cells expressing TNF-alpha TGF-beta less extensive than mycobacteria. There a significant negative between number antigens, suggesting role amounts also showed greater those lower MPT64. conclusion, supports hypothesis that mechanism Correlation macrophage deactivating reduced suggests its pathogenesis bacillary persistence.