期刊
EXPERIMENTAL PARASITOLOGY
卷 128, 期 4, 页码 365-370出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.exppara.2011.04.007
关键词
IFN-gamma; TNF-alpha; IL-1; IL-6; Trypanosomosis
类别
The aim of this study was to measure the levels of interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), interleukin 1 (IL-1) and interleukin 6 (IL-6) in the serum of rats experimentally infected with Trypanosome evansi and to correlate these levels with hematological parameters. Initially, 48 rats (group T) were intraperitoneally inoculated with cryopreserved blood containing 1 x 10(6) trypomastigotes per animal. Twenty-eight animals (group C) were used as negative controls and received 0.2 mL of saline by the same route. The experimental groups were formed according to the time after infection and the degree of parasitemia as follows: four control subgroups (C3, C5, C10 and C20) with seven non-inoculated animals each and four test subgroups (T3, T5, T10 and T20) with 10 animals each inoculated with T. evansi. The blood samples were collected by cardiac puncture at days 3 (C3, 13), 5 (C5, T5), 10 (C10, T10) and 20 (C20, 120) post-infection (PI) to perform the complete blood count and the determination of IFN-gamma, TNF-alpha, IL-1 and IL-6 levels using an ELISA quantitative sandwich. Infected rats showed normocytic normochromic anemia during the experimental period. T. evansi infection in rats caused a serum increase (P < 0.01) of IFN-gamma, TNF-alpha, IL-1 and IL-6 levels at days 3, 5, 10 and 20 PI compared to the controls. The multiple linear regressions showed a reduction of 24% in the hematocrit as a consequence of the increased IFN-gamma, TNF-alpha and IL-1. Therefore, we conclude that the infection caused by T. evansi causes an increase in the pro-inflammatory cytokines. These results suggest a synergism among IL-1, TNF-alpha and IFN-gamma contributing to the development of anemia. This increase is associated with the regulation of immune responses against the parasite. (C) 2011 Elsevier Inc. All rights reserved.
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