Spontaneous neutrophil activation in HTLV-1 infected patients

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Abstract

Human T cell lymphotropic Virus type-1 (HTLV-1) induces lymphocyte activation and proliferation, but little is known about the innate immune response due to HTLV-1 infection. We evaluated the percentage of neutrophils that metabolize Nitroblue tetrazolium (NBT) to formazan in HTLV-1 infected subjects and the association between neutrophil activation and IFN-γ and TNF-α levels. Blood was collected from 35 HTLV-1 carriers, from 8 patients with HAM/TSP (HTLV-1-associated myelopathy); 22 healthy individuals were evaluated for spontaneous and lipopolysaccharide (LPS)-stimulated neutrophil activity (reduction of NBT to formazan). The production of IFN-γ and TNF-α by unstimulated mononuclear cells was determined by ELISA. Spontaneous NBT levels, as well as spontaneous IFN-γ and TNF-α production, were significantly higher (p<0.001) in HTLV-1 infected subjects than in healthy individuals. A trend towards a positive correlation was noted, with increasing percentage of NBT positive neutrophils and levels of IFN-γ. The high IFN-γ producing HTLV-1 patient group had significantly greater NBT than healthy controls, 43±24% and 17±4.8% respectively (p<0.001), while no significant difference was observed between healthy controls and the low IFN-γ-producing HTLV-1 patient group (30±20%). Spontaneous neutrophil activation is another marker of immune perturbation resulting from HTLV-1 infection. In vivo activation of neutrophils observed in HTLV-1 infected subjects is likely to be the same process that causes spontaneous IFN-γ production, or it may partially result from direct IFN-γ stimulation. © 2005 by The Brazilian Journal of Infectious Diseases and Contexto Publishing. All rights reserved.

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APA

Guerreiro, J. B., Porto, M. A. F., Santos, S. B., Lacerda, L., Ho, J. L., & Carvalho, E. M. (2005). Spontaneous neutrophil activation in HTLV-1 infected patients. Brazilian Journal of Infectious Diseases, 9(6), 510–514. https://doi.org/10.1590/S1413-86702005000600010

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