Host response to Brucella infection: review and future perspective

被引:48
作者
Elfaki, Mohamed G. [1 ,2 ]
Alaidan, Alwaleed Abdullah [1 ]
Al-Hokail, Abdullah Abdulrahman [2 ,3 ]
机构
[1] King Faisal Specialist Hosp & Res Ctr, Dept Infect & Immun, Riyadh 11211, Saudi Arabia
[2] Alfaisal Univ, Coll Med, Riyadh, Saudi Arabia
[3] King Faisal Specialist Hosp & Res Ctr, Dept Med, Riyadh 11211, Saudi Arabia
关键词
brucellosis; pathogenesis; immunity; Saudi Arabia; GAMMA-INTERFERON; ABORTUS; MELITENSIS; VIRULENT; MACROPHAGE; PROTEINS; DISCRIMINATE; DEFICIENT; DIAGNOSIS; BACTERIA;
D O I
10.3855/jidc.6625
中图分类号
R51 [传染病];
学科分类号
100401 ;
摘要
Brucellosis is a zoonotic and contagious infectious disease caused by infection with Brucella species. The infecting brucellae are capable of causing a devastating multi-organ disease in humans with serious health complications. The pathogenesis of Brucella infection is influenced largely by host factors, Brucella species/strain, and the ability of invading brucellae to survive and replicate within mononuclear phagocytic cells, preferentially macrophages (M.). Consequently, the course of human infection may appear as an acute fatal or progress into chronic debilitating infection with periodical episodes that leads to bacteremia and death. The existence of brucellae inside M. represents one of the strategies used by Brucella to evade the host immune response and is responsible for treatment failure in certain human populations treated with anti-Brucella drugs. Moreover, the persistence of brucellae inside M. complicates the diagnosis and may affect the host cell signaling pathways with consequent alterations in both innate and adaptive immune responses. Therefore, there is an urgent need to pursue the development of novel drugs and/or vaccine targets against human brucellosis using high throughput technologies in genomics, proteomics, and immunology.
引用
收藏
页码:697 / 701
页数:5
相关论文
共 50 条
[41]   PATHOGENESIS OF BRUCELLA [J].
SMITH, LD ;
FICHT, TA .
CRITICAL REVIEWS IN MICROBIOLOGY, 1990, 17 (03) :209-230
[43]   T lymphocyte mediated protection against facultative intracellular bacteria [J].
Splitter, G ;
Oliveira, S ;
Carey, M ;
Miller, C ;
Ko, J ;
Covert, J .
VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY, 1996, 54 (1-4) :309-319
[44]   EFFECTS OF GAMMA-INTERFERON AND INDOMETHACIN IN PREVENTING BRUCELLA-ABORTUS INFECTIONS IN MICE [J].
STEVENS, MG ;
PUGH, GW ;
TABATABAI, LB .
INFECTION AND IMMUNITY, 1992, 60 (10) :4407-4409
[45]   CD4+ T Cell-derived IL-10 Promotes Brucella abortus Persistence via Modulation of Macrophage Function [J].
Xavier, Mariana N. ;
Winter, Maria G. ;
Spees, Alanna M. ;
Kim Nguyen ;
Atluri, Vidya L. ;
Silva, Teane M. A. ;
Baeumler, Andreas J. ;
Mueller, Werner ;
Santos, Renato L. ;
Tsolis, Renee M. .
PLOS PATHOGENS, 2013, 9 (06)
[46]  
Yagupsky P, 2000, SCAND J INFECT DIS, V32, P31, DOI 10.1080/00365540050164182
[47]  
YOUNG EJ, 1983, REV INFECT DIS, V5, P821
[48]   HUMAN PERIPHERAL-BLOOD CD4(+) AND CD8(+) T-CELLS EXPRESS TH1-LIKE CYTOKINE MESSENGER-RNA AND PROTEINS FOLLOWING IN-VITRO STIMULATION WITH HEAT-INACTIVATED BRUCELLA-ABORTUS [J].
ZAITSEVA, MB ;
GOLDING, H ;
BETTS, M ;
YAMAUCHI, A ;
BLOOM, ET ;
BUTLER, LE ;
STEVAN, L ;
GOLDING, B .
INFECTION AND IMMUNITY, 1995, 63 (07) :2720-2728
[49]   Tumor necrosis factor alpha and interleukin-12 contribute to resistance to the intracellular bacterium Brucella abortus by different mechanisms [J].
Zhan, YF ;
Liu, ZQ ;
Cheers, C .
INFECTION AND IMMUNITY, 1996, 64 (07) :2782-2786
[50]   DIFFERENTIAL INDUCTION OF MACROPHAGE-DERIVED CYTOKINES BY LIVE AND DEAD INTRACELLULAR BACTERIA IN-VITRO [J].
ZHAN, YF ;
CHEERS, C .
INFECTION AND IMMUNITY, 1995, 63 (02) :720-723