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ROS-deficient monocytes have aberrant gene expression that correlates with inflammatory disorders of chronic granulomatous disease

Journal article
Authors Kelly Brown
Johan Bylund
K. L. Macdonald
G. X. Song-Zhao
M. R. Elliott
R. Falsafi
R. E. Hancock
D. P. Speert
Published in Clin Immunol
Volume 129
Issue 1
Pages 90-102
ISSN 1521-7035 (Electronic)
Publication year 2008
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Pages 90-102
Language en
Links www.ncbi.nlm.nih.gov/entrez/query.f...
Keywords Adolescent, Adult, Cytokines/biosynthesis/*genetics/immunology, Extracellular Signal-Regulated MAP Kinases/metabolism, Gene Expression Profiling, Granulomatous Disease, Chronic/genetics/*immunology/metabolism, Humans, Inflammation Mediators/immunology/*metabolism, Male, Monocytes/*immunology/metabolism, Oligonucleotide Array Sequence Analysis, Protein-Serine-Threonine Kinases/metabolism, Reactive Oxygen Species/*metabolism, Signal Transduction, Toll-Like Receptors/*immunology, p38 Mitogen-Activated Protein Kinases/metabolism
Subject categories Medical and Health Sciences

Abstract

Chronic granulomatous disease is an immunodeficiency caused by an inability to produce reactive oxygen species. While the mechanism of hyper-sensitivity to infection is well understood in CGD, the basis for debilitating inflammatory disorders that arise in the absence of evident infection has not been fully explained. Herein it is demonstrated that resting and TLR-activated monocytes from individuals with CGD expressed significantly higher levels of inflammatory mediators than control cells; the expression in CGD cells resembled normal cells stimulated with lipopolysaccharide. The lack of acute illness, infection or circulating endotoxin in the blood of the CGD patients at the time of sampling was consistent with infection-free inflammation. The enhanced expression of inflammatory mediators correlated with elevated expression of NF-kappaB and was dependent on ERK1/2 signalling. The results are consistent with the hypothesis that ROS are anti-inflammatory mediators that control gene expression and potentially limit the development of sterile inflammatory disorders.

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