Analysis of the immune response in infections of the goldfish (Carassius auratus L.) with Mycobacterium marinum

被引：29
作者：
Hodgkinson, Jordan W. [1 ]
Ge, Jun-Qing [1 ,3 ]
Grayfer, Leon [1 ]
Stafford, James [1 ]
Belosevic, Miodrag [1 ,2 ]
机构：
[1] Univ Alberta, Dept Biol Sci, Edmonton, AB T6G 2E9, Canada
[2] Univ Alberta, Sch Publ Hlth, Edmonton, AB T6G 2E9, Canada
[3] Fujian Acad Agr Sci, Inst Biotechnol, Fuzhou, Fijian, Peoples R China
来源：
DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY | 2012年 / 38卷 / 03期
基金：
加拿大自然科学与工程研究理事会;
关键词：
Mycobacteria; Fish; Macrophage; Respiratory burst; Nitric oxide; NADPH; iNOS; Cytokines; Cytokine receptors; NITRIC-OXIDE SYNTHASE; FUNCTIONAL-ANALYSIS; INTERFERON-GAMMA; MOLECULAR CHARACTERIZATION; ANTIMICROBIAL RESPONSES; PHAGOSOME MATURATION; LATENT TUBERCULOSIS; REACTIVE OXYGEN; ANIMAL-MODEL; IFN-GAMMA;
D O I：
10.1016/j.dci.2012.07.006
中图分类号：
S9 [水产、渔业];
学科分类号：
0908 ;
摘要：
The rapid doubling time and genetic relatedness of the fish pathogen Mycobacterium marinum to Mycobacterium tuberculosis has rendered the former an attractive model for investigating mycobacterial host-. pathogen interactions. We employed the M. marinum-goldfish infection model to investigate the in vivo immune responses to this pathogen in the context of a natural host. Histological analysis revealed mycobacterial infiltrates in goldfish kidney and spleen tissues, peaking 28 days post infections (dpi). Quantitative gene expression analysis showed significant increases of mRNA levels of pro-inflammatory cytokines (IFN gamma, IL-12p40, IL-1 beta 1) and cytokine receptors (IFNGR1-1, TNFR2) at 7 dpi. Conversely, the gene expression levels of key anti-inflammatory cytokines TGF beta and IL-10 were elevated at 14 dpi. Furthermore. M. marinum infections markedly increased the cytokine-primed oxidative burst responses of isolated kidney phagocytes at 7 but not 56 dpi. We believe that the M. marinum-goldfish infection model will be invaluable in furthering the understanding of the mycobacterium host-pathogen interface. (C) 2012 Elsevier Ltd. All rights reserved.
引用
收藏
页码：456 / 465
页数：10
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