Mycobacterium avium uses apoptotic macrophages as tools for spreading

被引:59
作者
Early, Julie [1 ,2 ]
Fischer, Kay [1 ]
Bermudez, Luiz E. [1 ,2 ,3 ]
机构
[1] Oregon State Univ, Dept Biomed Sci, Coll Vet Med, Corvallis, OR 97331 USA
[2] Oregon State Univ, Program Mol & Cell Biol, Corvallis, OR 97331 USA
[3] Oregon State Univ, Dept Microbiol, Coll Sci, Corvallis, OR 97331 USA
关键词
Mycobacterium avium; Macrophages; Apoptosis; Spread; Escape; ARGININE TRANSLOCATION PATHWAY; PROGRAMMED CELL-DEATH; INFECTED MACROPHAGES; PSEUDOMONAS-SYRINGAE; PHAGOSOME MATURATION; BEIGE MICE; IFN-GAMMA; VIRULENCE; DISSEMINATION; TUBERCULOSIS;
D O I
10.1016/j.micpath.2010.12.004
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Background: Mycobacterium avium (MAC) lives and replicates in macrophages and causes disseminated disease in immunocompromised individuals. As a host response to control disease, many macrophages become apoptotic a few days after MAC infection. In this study, we hypothesized that MAC can survive autophagic and apoptotic macrophages and spread. Methods: Electron, time-lapse video, fluorescence microscopy. Apoptosis was determined by ELISA and TUNEL assays. Autophagy was seen by migration of LC3-1. Results: Apoptotic macrophages harbor chiefly viable MAC. MAC escapes both the vacuole and the macrophage once apoptosis is triggered, leaving the bacteria free to infect nearby macrophages in the process of spreading. In addition, some MAC species will have apoptotic bodies and are released in healthy macrophages following apoptotic body ingestion. Because autophagy precedes apoptosis, it was established that heat-killed MAC, and viable MAC induces autophagy in macrophages at similar rates, but MAC still survives. Conclusion: MAC spreading from cell-to-cell is triggered by the macrophage's attempt to kill the bacterium, undergoing apoptosis. (C) 2010 Elsevier Ltd. All rights reserved.
引用
收藏
页码:132 / 139
页数:8
相关论文
共 41 条
[1]   SUSCEPTIBILITY OF BEIGE MICE TO MYCOBACTERIUM-AVIUM - ROLE OF NEUTROPHILS [J].
APPELBERG, R ;
CASTRO, AG ;
GOMES, S ;
PEDROSA, J ;
SILVA, MT .
INFECTION AND IMMUNITY, 1995, 63 (09) :3381-3387
[2]  
Barker LP, 1999, FEMS MICROBIOL LETT, V175, P79, DOI 10.1016/S0378-1097(99)00169-X
[3]   pH-dependent perforation of macrophage phagosomes by listeriolysin O from Listeria monocytogenes [J].
Beauregard, KE ;
Lee, KD ;
Collier, RJ ;
Swanson, JA .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 186 (07) :1159-1163
[4]   A common export pathway for proteins binding complex redox cofactors? [J].
Berks, BC .
MOLECULAR MICROBIOLOGY, 1996, 22 (03) :393-404
[5]   Intracellular phenotype of Mycobacterium avium enters macrophages primarily by a macropinocytosis-like mechanism and survives in a compartment that differs from that with extracellular phenotype [J].
Bermudez, LE ;
Petrofsky, M ;
Sangari, F .
CELL BIOLOGY INTERNATIONAL, 2004, 28 (05) :411-419
[6]   Growth within macrophages increases the efficiency of Mycobacterium avium in invading other macrophages by a complement receptor-independent pathway [J].
Bermudez, LE ;
Parker, A ;
Goodman, JR .
INFECTION AND IMMUNITY, 1997, 65 (05) :1916-1925
[7]  
BERMUDEZ LEM, 1988, J IMMUNOL, V140, P3006
[8]   Identification of a twin-arginine translocation system in Pseudomonas syringae pv. tomato DC3000 and its contribution to pathogenicity and fitness [J].
Bronstein, PA ;
Marrichi, M ;
Cartinhour, S ;
Schneider, DJ ;
DeLisa, MP .
JOURNAL OF BACTERIOLOGY, 2005, 187 (24) :8450-8461
[9]   The tat pathway of the plant pathogen Pseudomonas syringae is required for optimal virulence [J].
Caldelari, I ;
Mann, S ;
Crooks, C ;
Palmer, T .
MOLECULAR PLANT-MICROBE INTERACTIONS, 2006, 19 (02) :200-212
[10]   Protein secretion systems in Mycobacteria [J].
Champion, Patricia A. DiGiuseppe ;
Cox, Jeffery S. .
CELLULAR MICROBIOLOGY, 2007, 9 (06) :1376-1384