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Analyse of genes expression of the Bcl-2 family in macrophages infected for uni and multi-drugs resistance Mycobacterium tuberculosis Tuberculsis, an ancient infection disease, continues to thrive. Although well described, it remains a world health problem to overcome. The development and application of new strategies to control Tuberculosis requires a better understanding of mechanisms involved in mycobacteria-macrophages interaction. Following phagocytosis, mycobacteria initiates a variety of actions to survive and multiply themselves inside macrophages. According to researches, mycobacteria might interfere in the cell death mechanism. This ability became a challenge to be studied due to its implications in the pathogenesis of the disease. The aim of this study was to analyze the gene expression of anti-apoptotic (bcl-2 ̧ bcl-x e mcl-1) and pro-apoptotic genes (bak, bax e bid) in PMA-treated THP-1 cells by Real Time qPCR. Moreover, the percentage of macrophage DNA fragmentation was assessed by flow citometry because internucleosomal DNA fragmentation is characteristic of apoptotic and pyroptotic cell death. The infection was carried out using clinical isolates of M. tuberculosis resistent to multiple drugs, drug susceptibility and the M. tuberculosis H37Rv strain. The difference in the expression profile among clinical isolates, susceptible and resistant to three drugs used in the TB treatment, and the M. tuberculosis H37Rv were evaluated with the method 2. In order to compare gene expression patterns as well as the percentage of DNA fragmentation in macrophages infected with different clinical isolates, it was used analysis of variance (ANOVA) and Tukey`s multiple comparison test. The results suggest that M. tuberculosis H37Rv and the clinical isolates presenting higher drug resistant profile might induce programmed cell death in macrophages after 24-h infection. This was observed in the gene expression pattern and also in the macrophage DNA fragmentation profile, which indentifies apoptosis or pyroptosis. Therefore, it is suggested these clinical isolates and M. tuberculosis H37Rv do not present anti-apoptotic mechanisms to evade immune response. Moreover, the infection time is an important factor and, definitely, infections for long time could induce increase death of the infectados macrophages.

Análise da expressão de genes da família Bcl-2 em macrófagos infectados por Mycobacterium tuberculosis uni e multi-drogas resistentes