Cellular responses and cytokine production in post-treatment hookworm patients from an endemic area in Brazil

被引:80
作者
Geiger, SM
Massara, CL
Bethony, J
Soboslay, PT
Corrêa-Oliveira, R
机构
[1] Fdn Oswaldo Cruz, Ctr Pesquisas Rene Rachou, Lab Imunol, Belo Horizonte, MG, Brazil
[2] Univ Tubingen, Inst Trop Med, Tubingen, Germany
[3] George Washington Univ, Dept Microbiol & Trop Med, Washington, DC USA
关键词
cellular reactivity; cytokines; hookworm infection; Necator americanus; schoolchildren;
D O I
10.1111/j.1365-2249.2004.02449.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Human hookworm infections are distributed widely in tropical areas and have a significant impact on host morbidity and human health. In the present study, we investigated the cellular responsiveness and cytokine production in peripheral blood mononuclear cells (PBMC) from Necator americanus-infected schoolchildren who had recently received chemotherapy, and compared them with non-infected endemic controls. Hookworm patients and treated, egg-negative individuals showed a lower cellular reactivity against phytohaemagglutinin (PHA) and hookworm antigen when compared with egg-negative endemic controls. The baseline production of proinflammatory tumour necrosis factor-alpha (TNF-alpha) in PBMC from infected patients and treated, egg-negative individuals was elevated. On the other hand, PHA- or hookworm antigen-induced interleukin (IL)-12 and interferon (IFN)-gamma secretion was higher in endemic controls than in hookworm patients, who either continued egg-positive or were egg-negative after treatment. Also, PBMC from endemic controls secreted more IL-5 and IL-13 than the other patient groups. Opposite to that, the spontaneous as well as the antigen-driven IL-10 secretion was lower in endemic controls when compared with the other groups. In summary, patently hookworm-infected as well as egg-negative treated patients disclosed an elevated spontaneous cellular secretion of proinflammatory TNF-alpha, a prominent secretion of regulatory Th2-type IL-10 and an impaired production of IL-12, IFN-gamma, IL-5 and IL-13.
引用
收藏
页码:334 / 340
页数:7
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