Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/69065
Type: Artigo de periódico
Title: Hyperresponsiveness of neutrophils from gp 91(phox) deficient patients to lipopolysaccharide and serum amyloid A
Author: Hatanaka, E
Carvalho, BTC
Condino-Neto, A
Campa, A
Abstract: We demonstrate here that neutrophils from chronic granulomatous disease (CGD) patients release larger amounts of interleukin-8 (IL-8) and tumor necrosis factor alpha (TNF-alpha) than neutrophils from control subjects. Incremental cytokine production was observed under both basal and stimulated conditions in neutrophils from two CGD (gp 91(phox)) patients. The basal production of IL-8 was over seven-fold greater in CGD patients. The two samples assayed showed 3- and 10-fold increases in TNF-alpha. Basically, the same magnitude of increment was observed in lypopolysaccharide (LPS) and serum amyloid A protein (SAA)-stimulated cells. We also found that the levels of SAA and IL-8 were higher in the serum of CGD patients than the levels found in the serum of healthy donors. The increased responsiveness of neutrophils from CGD patients may be closely related with a deficiency in the assembly of the nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase enzyme system, or it may be due to a frequent inflammatory condition in these patients. In the latter case, the increased serum levels of systemic inflammatory factors, among them SAA, would contribute to the sustained accumulation and activation of phagocytes. Whatever the origin, the excessive production of cytokines may lead to inappropriate activation and tissue injury and even to increased susceptibility to invasive microorganisms, impairing the quality life of CGD patients. (C) 2004 Elsevier B.V. All rights reserved.
Subject: IL-8
TNF-alpha
CGD
neutrophils
SAA
Country: Holanda
Editor: Elsevier Science Bv
Rights: fechado
Identifier DOI: 10.1016/j.imlet.2004.04.016
Date Issue: 2004
Appears in Collections:Unicamp - Artigos e Outros Documentos

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