Salmonellosis: Host immune responses and bacterial virulence determinants

被引:312
作者
Jones, BD
Falkow, S
机构
[1] NIH, ROCKY MT LABS, MICROSCOPY BRANCH, HAMILTON, MT 59840 USA
[2] STANFORD UNIV, SCH MED, DEPT MICROBIOL & IMMUNOL, STANFORD, CA 94305 USA
关键词
typhoid fever; macrophage survival; M cells; bacterial invasion; Salmonella;
D O I
10.1146/annurev.immunol.14.1.533
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The lifestyle of bacterial pathogens requires them to establish infection in the face of host immunity. Upon entering a potential host, a variety of interactions are initiated, the outcome of which depends upon a myriad of attributes of each of the participants. In this review we discuss the interactions that occur between pathogenic Salmonella species and the host immune systems, but when appropriate to broaden perspective, we have provided a general overview of the interactions between bacterial pathogens and animal hosts. Pathogenic Salmonella species possess an array of invasion genes that produce proteins secreted by a specialized type III secretion apparatus, These proteins are used by the bacteria to penetrate the intestinal mucosa by invading and destroying specialized epithelial M cells of the Peyer's patches. This manuever deposits the bacteria directly within the confines of the reticuloendothelial system. The host responds to these actions with nonspecific phagocytic cells and an imflammatory response as well as by activating specific cellular and humoral immune responses. Salmonella responds to this show of force directly. It appears that the bacteria invade and establish a niche within the very cells that have been sent to destroy them. Efforts are underway to characterize the factors that allow these intracellular bacteria to customize intracellular vacuoles for their own purposes. It is the constant play between these interactions that determines the outcome of the host infection, and clearly they will also shape the evolution of new survival strategies for both the bacterium and the host.
引用
收藏
页码:533 / 561
页数:29
相关论文
共 156 条
  • [1] GROWTH-RATE PARADOX OF SALMONELLA-TYPHIMURIUM WITHIN HOST MACROPHAGES
    ABSHIRE, KZ
    NEIDHARDT, FC
    [J]. JOURNAL OF BACTERIOLOGY, 1993, 175 (12) : 3744 - 3748
  • [2] PREVENTION OF TYPHOID-FEVER IN NEPAL WITH THE VI CAPSULAR POLYSACCHARIDE OF SALMONELLA-TYPHI - A PRELIMINARY-REPORT
    ACHARYA, IL
    LOWE, CU
    THAPA, R
    GURUBACHARYA, VL
    SHRESTHA, MB
    CADOZ, M
    SCHULZ, D
    ARMAND, J
    BRYLA, DA
    TROLLFORS, B
    CRAMTON, T
    SCHNEERSON, R
    ROBBINS, JB
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1987, 317 (18) : 1101 - 1104
  • [3] AKIYAMA T, 1987, J BIOL CHEM, V262, P5592
  • [4] PROKARYOTIC SIGNAL TRANSDUCTION MEDIATED BY SENSOR AND REGULATOR PROTEIN PAIRS
    ALBRIGHT, LM
    HUALA, E
    AUSUBEL, FM
    [J]. ANNUAL REVIEW OF GENETICS, 1989, 23 : 311 - 336
  • [5] SALMONELLA STIMULATE MACROPHAGE MACROPINOCYTOSIS AND PERSIST WITHIN SPACIOUS PHAGOSOMES
    ALPUCHEARANDA, CM
    RACOOSIN, EL
    SWANSON, JA
    MILLER, SI
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 1994, 179 (02) : 601 - 608
  • [6] IMMUNOSUPPRESSION INDUCED BY NITRIC-OXIDE AND ITS INHIBITION BY INTERLEUKIN-4
    ALRAMADI, BK
    MEISSLER, JJ
    HUANG, D
    EISENSTEIN, TK
    [J]. EUROPEAN JOURNAL OF IMMUNOLOGY, 1992, 22 (09) : 2249 - 2254
  • [7] CLONING AND MOLECULAR CHARACTERIZATION OF A GENE INVOLVED IN SALMONELLA ADHERENCE AND INVASION OF CULTURED EPITHELIAL-CELLS
    ALTMEYER, RM
    MCNERN, JK
    BOSSIO, JC
    ROSENSHINE, I
    FINLAY, BB
    GALAN, JE
    [J]. MOLECULAR MICROBIOLOGY, 1993, 7 (01) : 89 - 98
  • [8] SALMONELLA-TYPHIMURIUM ACTIVATES VIRULENCE GENE-TRANSCRIPTION WITHIN ACIDIFIED MACROPHAGE PHAGOSOMES
    ARANDA, CMA
    SWANSON, JA
    LOOMIS, WP
    MILLER, SI
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (21) : 10079 - 10083
  • [9] BAJAJ V, 1996, IN PRESS MOL MICROBI
  • [10] Bao Xinghao, 1992, Acta Microbiologica Sinica, V32, P289