Document Detail


Uric acid, a nucleic acid degradation product, down-regulates dsRNA-triggered arthritis.
MedLine Citation:
PMID:  16387838     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Uric acid, the naturally occurring degradation product of purine metabolism, is a danger signal, driving maturation of dendritic cells. It is well known that uric acid crystals display potent proinflammatory properties--the cause of gout--whereas the biological properties of soluble uric acid are less well documented. We have demonstrated previously that nucleic acids of endogenous and exogenous origin display proinflammatory properties. The aim of the present study was to assess the impact of soluble uric acid on in vivo inflammatory responses. Mice were administered with uric acid suspension in saline or saline alone prior to induction of neutrophil-mediated inflammation, delayed-type hypersensitivity, histamin-induced edema (measure of vasodilation capacity), as well as double-stranded (ds)RNA-triggered arthritis. Frequency and severity of arthritis were decreased significantly in mice exposed to dsRNA and simultaneously treated with uric acid as compared with saline-treated controls. Also, granulocyte-mediated inflammatory response and vasodilation capacity were reduced significantly in mice treated with uric acid as compared with their control group. The data suggest that down-regulation of inflammation was mediated by skewing the inflammatory response from the peripheral sites to the peritoneal cavity and down-regulating vasodilatatory capacity and thereby affecting leukocyte migration. In contrast, the T cell-mediated delayed-type hypersensitivity reaction was not affected significantly in mice exposed to uric acid. These findings demonstrate that uric acid displays a potent, distant anti-inflammatory effect in vivo. This property seems to be mediated by down-regulation of neutrophil influx to the site of inflammatory insult.
Authors:
Fariba Zare; Mattias Magnusson; Tomas Bergström; Mikael Brisslert; Elisabet Josefsson; Anna Karlsson; Andrej Tarkowski
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2005-12-30
Journal Detail:
Title:  Journal of leukocyte biology     Volume:  79     ISSN:  0741-5400     ISO Abbreviation:  J. Leukoc. Biol.     Publication Date:  2006 Mar 
Date Detail:
Created Date:  2006-03-01     Completed Date:  2006-05-02     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8405628     Medline TA:  J Leukoc Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  482-8     Citation Subset:  IM    
Affiliation:
Department of Rheumatology and Inflammation Research, University of Göteborg, Sweden. fariba.zare@rheuma.gu.se
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MeSH Terms
Descriptor/Qualifier:
Animals
Arthritis, Experimental / chemically induced,  drug therapy,  immunology*
Chemotaxis / drug effects,  immunology
Chemotaxis, Leukocyte / drug effects,  immunology
Disease Models, Animal
Down-Regulation / drug effects,  immunology*
Edema / chemically induced,  immunology,  physiopathology
Female
Hypersensitivity, Delayed / chemically induced,  immunology,  physiopathology
Immunosuppressive Agents / immunology*,  metabolism,  pharmacology
Inflammation Mediators / adverse effects,  immunology
Joints / drug effects,  immunology,  physiopathology
Mice
Neutrophils / drug effects,  immunology
Nucleic Acids / immunology*,  metabolism
RNA, Double-Stranded / adverse effects,  immunology*
Uric Acid / immunology*,  metabolism,  pharmacology
Vasodilation / drug effects,  immunology
Chemical
Reg. No./Substance:
0/Immunosuppressive Agents; 0/Inflammation Mediators; 0/Nucleic Acids; 0/RNA, Double-Stranded; 69-93-2/Uric Acid

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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