TY - JOUR
T1 - Apoptosis of human monocytes/macrophages in Mycobacterium tuberculosis infection
AU - Placido, Roberta
AU - Mancino, Giorgio
AU - Amendola, Alessandra
AU - Mariani, Francesca
AU - Vendetti, Silvia
AU - Piacentini, Mauro
AU - Sanduzzi, Alessandro
AU - Bocchino, Maria Luisa
AU - Zembala, Marek
AU - Colizzi, Vittorio
PY - 1997/1
Y1 - 1997/1
N2 - Tuberculosis (TB) is still a major health problem, both as a single disease entity and as a cofactor in AIDS. The interaction between macrophage and Mycobacterium tuberculosis (MTB) is a critical step in the establishment of an early chronic infection. This study analyses the capacity of MTB to induce apoptosis in cells obtained by broncho-alveolar lavage (BAL) from patients with reactive pulmonary tuberculosis and from AIDS patients with disseminated pulmonary tuberculosis. Apoptosis was increased three-fold in BAL cells obtained from patients with pulmonary tuberculosis and even more markedly in alveolar macrophages of MTB-infected AIDS patients, compared with controls. Apoptosis was analysed and characterized by propidium iodide (PI) incorporation, terminal deoxy transferase (TDT)-mediated dUTP-biotin nick end labelling (TUNEL), and tissue transglutaminase (tTG) expression. The MTB-macrophage interaction was also investigated in vitro by infecting monocyte-derived macrophages (MDM) with MTB (virulent strain H37Rv). The induction of apoptosis by MTB required viable bacteria, was dose-dependent, and was restricted to H37Rv. Infection with either Mycobacterium avium complex (MAC) or HIV-1 and treatment with heat-killed MTB failed to induce apoptosis.
AB - Tuberculosis (TB) is still a major health problem, both as a single disease entity and as a cofactor in AIDS. The interaction between macrophage and Mycobacterium tuberculosis (MTB) is a critical step in the establishment of an early chronic infection. This study analyses the capacity of MTB to induce apoptosis in cells obtained by broncho-alveolar lavage (BAL) from patients with reactive pulmonary tuberculosis and from AIDS patients with disseminated pulmonary tuberculosis. Apoptosis was increased three-fold in BAL cells obtained from patients with pulmonary tuberculosis and even more markedly in alveolar macrophages of MTB-infected AIDS patients, compared with controls. Apoptosis was analysed and characterized by propidium iodide (PI) incorporation, terminal deoxy transferase (TDT)-mediated dUTP-biotin nick end labelling (TUNEL), and tissue transglutaminase (tTG) expression. The MTB-macrophage interaction was also investigated in vitro by infecting monocyte-derived macrophages (MDM) with MTB (virulent strain H37Rv). The induction of apoptosis by MTB required viable bacteria, was dose-dependent, and was restricted to H37Rv. Infection with either Mycobacterium avium complex (MAC) or HIV-1 and treatment with heat-killed MTB failed to induce apoptosis.
KW - macrophage
KW - Mycobacterium tuberculosis
KW - tuberculosis
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U2 - 10.1002/(SICI)1096-9896(199701)181:1<31::AID-PATH722>3.0.CO;2-G
DO - 10.1002/(SICI)1096-9896(199701)181:1<31::AID-PATH722>3.0.CO;2-G
M3 - Article
C2 - 9072000
AN - SCOPUS:0031038856
VL - 181
SP - 31
EP - 38
JO - Journal of Pathology
JF - Journal of Pathology
SN - 0022-3417
IS - 1
ER -