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

SUMMARY 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‐...

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Veröffentlicht in:Clinical and experimental immunology 2004-05, Vol.136 (2), p.334-340
Hauptverfasser: GEIGER, S. M., MASSARA, C. L., BETHONY, J., SOBOSLAY, P. T., CORRÊA‐OLIVEIRA, R.
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Sprache:eng
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Zusammenfassung:SUMMARY 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‐α (TNF‐α) 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)‐γ 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‐α, a prominent secretion of regulatory Th2‐type IL‐10 and an impaired production of IL‐12, IFN‐γ, IL‐5 and IL‐13.
ISSN:0009-9104
1365-2249
DOI:10.1111/j.1365-2249.2004.02449.x