Dominant Th1 cytokine production in early onset of human brucellosis followed by switching towards Th2 along prolongation of disease

被引:64
作者
Rafiei, Alireza
Ardestani, Sussan K. [1 ]
Kariminia, Amina
Keyhani, Abdolhosein
Mohraz, Mino
Amirkhani, Aref
机构
[1] Univ Tehran, Inst Biochem & Biophys, Immunol Sect, Tehran, Iran
[2] Mazandaran Univ Med Sci, Sari Med Sch, Dept Immunol & Microbiol, Sari, Iran
[3] Inst Pasteur, Dept Immunol, Tehran, Iran
[4] Univ Tehran Med Sci, Fac Med, Dept Immunol, Tehran, Iran
[5] Univ Tehran Med Sci, Sch Med, Dept Infect Dis, Tehran, Iran
[6] Pasteur Inst Iran, Dept Epidemiol, Tehran, Iran
关键词
human brucellosis; IFN-gamma; IL-13;
D O I
10.1016/j.jinf.2005.11.024
中图分类号
R51 [传染病];
学科分类号
100401 ;
摘要
Human brucellosis is a worldwide zoonotic infectious disease which is caused by intracellular bacteria belonging to the genus Brucella. Based on murine studies it has been shown that host resistance to Brucella depends on Th1 response, whereas Th2 response is involved in the severity of the disease. Since the immune response during human brucellosis has not been profoundly studied we have tried to evaluate cytokine production in patients suffering from brucellosis. Diluted whole blood samples were cultured in the presence of the mitogen, heat inactivated bacteria or medium alone. IL-12, IFN-gamma and IL-10 were measured by specific sandwich ELISA. In addition, the percentage of CD3(+) T cells producing either IL-13 or IFN-gamma was determined by flow cytometry. It was found that not only IFN-gamma production but also the number of CD3(+) IFN-gamma-producing cells decreased with prolongation of the disease but the percentage of CD3(+) IL-13(+) T cells were significantly increased. No correlation between duration of disease and IL-10 or IL-12 production was found. In conclusion, it is proposed that at the onset of brucellosis, Th1 response dominates white diminishing with prolongation of the disease. (C) 2005 The British Infection Society. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:315 / 324
页数:10
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