Induction of apoptosis in murine macrophages by Mycobacterium tuberculosis is reactive oxygen intermediates-independent

被引:25
作者
Rojas, M [1 ]
Barrera, LF [1 ]
García, LF [1 ]
机构
[1] Univ Antioquia, Fac Med, Lab Cent Invest, Grp Inmunol Celular & Inmunogenet, Medellin, Colombia
关键词
reactive oxygen intermediates; reactive nitrogen intermediates; nitric oxide; apoptosis; Nramp1; murine macrophages; Mycobacterium tuberculosis;
D O I
10.1006/bbrc.1998.8802
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Infection with Mycobacterium tuberculosis induces apoptosis in murine macrophage lines. Resistant macrophages B10R (Bcg(r)) are more prone to undergo apoptosis than susceptible BIOS (Bcg(s)) macrophages. Apoptosis and inhibition of intracellular growth of the mycobacteria seem to be dependent on the production of nitric oxide, since both can be reverted by aminoguanidine (AMG). Although B10R macrophages produce more superoxide anion than BIOS macrophages after infection with M. tuberculosis, reactive oxygen intermediate (ROIs) scavengers did not affect uptake of H-3-uracil incorporation by the mycobacteria nor the induction of apoptosis, These results further suggest that both phenomena are dependent on the production of nitric oxide by the infected macrophages. (C) 1998 Academic Press.
引用
收藏
页码:436 / 442
页数:7
相关论文
共 48 条
[1]   Effector molecules in expression of the antimicrobial activity of macrophages against Mycobacterium avium complex: roles of reactive nitrogen intermediates, reactive oxygen intermediates, and free fatty acids [J].
Akaki, T ;
Sato, K ;
Shimizu, T ;
Sano, C ;
Kajitani, H ;
Dekio, S ;
Tomioka, H .
JOURNAL OF LEUKOCYTE BIOLOGY, 1997, 62 (06) :795-804
[2]   ENDOGENOUS INTERLEUKIN-10 PREVENTS APOPTOSIS IN MACROPHAGES DURING SALMONELLA INFECTION [J].
ARAI, T ;
HIROMATSU, K ;
NISHIMURA, H ;
KIMURA, Y ;
KOBAYASHI, N ;
ISHIDA, H ;
NIMURA, Y ;
YOSHIKAI, Y .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1995, 213 (02) :600-607
[3]   Inhibition of virulent Mycobacterium tuberculosis by Bcg(r) and Bcg(s) macrophages correlates with nitric oxide production [J].
Arias, M ;
Rojas, M ;
Zabaleta, J ;
Rodriguez, JI ;
Paris, SC ;
Barrera, LF ;
Garcia, LF .
JOURNAL OF INFECTIOUS DISEASES, 1997, 176 (06) :1552-1558
[4]   Apoptosis of monocytes and prolonged survival of granulocytes as a result of phagocytosis of bacteria [J].
Baran, J ;
Guzik, K ;
Hryniewicz, W ;
Ernst, M ;
Flad, HD ;
Pryjma, J .
INFECTION AND IMMUNITY, 1996, 64 (10) :4242-4248
[5]  
BARNES PF, 1992, J IMMUNOL, V149, P541
[6]  
BARRERA LF, 1994, IMMUNOLOGY, V82, P457
[7]   NRAMP TRANSFECTION TRANSFERS ITY/LSH/BCG-RELATED PLEIOTROPIC EFFECTS ON MACROPHAGE ACTIVATION - INFLUENCE ON OXIDATIVE BURST AND NITRIC-OXIDE PATHWAYS [J].
BARTON, CH ;
WHITEHEAD, SH ;
BLACKWELL, JM .
MOLECULAR MEDICINE, 1995, 1 (03) :267-279
[8]   GROWTH OF MYCOBACTERIUM-TUBERCULOSIS IN BCG-RESISTANT AND BCG-SUSCEPTIBLE MICE - ESTABLISHMENT OF LATENCY AND REACTIVATION [J].
BROWN, DH ;
MILES, BA ;
ZWILLING, BS .
INFECTION AND IMMUNITY, 1995, 63 (06) :2243-2247
[9]   Superoxide formation and macrophage resistance to nitric oxide-mediated apoptosis [J].
Brune, B ;
Gotz, C ;
Messmer, UK ;
Sandau, K ;
Hirvonen, MR ;
Lapetina, EG .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (11) :7253-7258
[10]   OXIDATIVE STRESS AS A MEDIATOR OF APOPTOSIS [J].
BUTTKE, TM ;
SANDSTROM, PA .
IMMUNOLOGY TODAY, 1994, 15 (01) :7-10