Progressive pulmonary tuberculosis is not due to increasing numbers of viable bacilli in rabbits, mice and guinea pigs, but is due to a continuous host response to mycobacterial products

被引:62
作者
Dannenberg, AM
Collins, FM
机构
[1] Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Environm Hlth Sci, Baltimore, MD USA
[2] Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Mol Microbiol & Immunol, Baltimore, MD USA
[3] Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Epidemiol, Baltimore, MD USA
[4] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA
[5] US FDA, Ctr Biol Evaluat & Res, Lab Mycobacterial Dis, Bethesda, MD USA
关键词
D O I
10.1054/tube.2001.0287
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Tuberculosis (TB) kills more people in the world today than any other infectious disease. A better vaccine to prevent clinical tuberculosis is greatly needed. Candidate vaccines are often evaluated by infecting rabbits, mice and guinea pigs by an aerosol of virulent tubercle bacilli and culturing their lungs for viable bacilli at various times thereafter. In all three species, however, the number of viable bacilli usually does not continuously increase until the host succumbs. The number of viable bacilli increases logarithmically for only about 3 weeks. Then, the host develops delayed-type hypersensitivity (DTH) and cell-mediated immunity (CMI), which keep the number of viable bacilli rather constant during the subsequent weeks. In the immunized host, DTH and CMI stop the logarithmic increase sooner than in the unimmunized controls, so that the stationary bacillary levels that follow are lower. This review analyzes host-parasite interactions in the lungs of rabbits, mice and guinea pigs. All three species cannot prevent inhaled fully virulent tubercle bacilli from establishing an infection, but they differ markedly in the type of the disease produced once it is established. (C) 2001 Harcourt Publishers Ltd.
引用
收藏
页码:229 / 242
页数:14
相关论文
共 106 条
[1]   Rabbit vascular endothelial adhesion molecules: ELAM-1 is most elevated in acute inflammation, whereas VCAM-1 and ICAM-1 predominate in chronic inflammation [J].
Abe, Y ;
Sugisaki, K ;
Dannenberg, AM .
JOURNAL OF LEUKOCYTE BIOLOGY, 1996, 60 (06) :692-703
[2]  
ALLISON MJ, 1962, AM REV RESPIR DIS, V85, P553
[3]  
ALSAADI AI, 1973, AM REV RESPIR DIS, V107, P1041
[4]  
[Anonymous], MICROBIOLOGY 1984
[5]  
[Anonymous], 1958, Tuberculosis in Animals and Man. A Study in Comparative Pathology
[6]   GROWTH-CHARACTERISTICS OF RECENT SPUTUM ISOLATES OF MYCOBACTERIUM-TUBERCULOSIS IN GUINEA-PIGS INFECTED BY THE RESPIRATORY ROUTE [J].
BALASUBRAMANIAN, V ;
WIEGESHAUS, EH ;
SMITH, DW .
INFECTION AND IMMUNITY, 1992, 60 (11) :4762-4767
[7]  
BARCLAY W R, 1970, Infection and Immunity, V2, P574
[8]  
BARCLAY WR, 1973, AM REV RESPIR DIS, V107, P351
[9]   Susceptibility of mice deficient in CD1D or TAP1 to infection with Mycobacterium tuberculosis [J].
Behar, SM ;
Dascher, CC ;
Grusby, MJ ;
Wang, CR ;
Brenner, MB .
JOURNAL OF EXPERIMENTAL MEDICINE, 1999, 189 (12) :1973-1980
[10]  
BLOOM BR, 1989, REV INFECT DIS, V11, pS460