Document Detail


Dietary glycine prevents peptidoglycan polysaccharide-induced reactive arthritis in the rat: role for glycine-gated chloride channel.
MedLine Citation:
PMID:  11500467     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Peptidoglycan polysaccharide (PG-PS) is a primary structural component of bacterial cell walls and causes rheumatoid-like arthritis in rats. Recently, glycine has been shown to be a potential immunomodulator; therefore, the purpose of this study was to determine if glycine would be protective in a PG-PS model of arthritis in vivo. In rats injected with PG-PS intra-articularly, ankle swelling increased 21% in 24 to 48 h and recovered in about 2 weeks. Three days prior to reactivation with PG-PS given intravenously (i.v.), rats were divided into two groups and fed a glycine-containing or nitrogen-balanced control diet. After i.v. PG-PS treatment joint swelling increased 2.1 +/- 0.3 mm in controls but only 1.0 +/- 0.2 mm in rats fed glycine. Infiltration of inflammatory cells, edema, and synovial hyperplasia in the joint were significantly attenuated by dietary glycine. Tumor necrosis factor alpha (TNF-alpha) mRNA was detected in ankle homogenates from rats fed the control diet but not in ankles from rats fed glycine. Moreover, intracellular calcium was increased significantly in splenic macrophages treated with PG-PS; however, glycine blunted the increase about 50%. The inhibitory effect of glycine was reversed by low concentrations of strychnine or chloride-free buffer, and it increased radiolabeled chloride influx nearly fourfold, an effect also inhibited by strychnine. In isolated splenic macrophages, glycine blunted translocation of the p65 subunit of NF-kappaB into the nucleus, superoxide generation, and TNF-alpha production caused by PG-PS. Further, mRNA for the beta subunit of the glycine receptor was detected in splenic macrophages. This work supports the hypothesis that glycine prevents reactive arthritis by blunting cytokine release from macrophages by increasing chloride influx via a glycine-gated chloride channel.
Authors:
X Li; B U Bradford; M D Wheeler; S A Stimpson; H M Pink; T A Brodie; J H Schwab; R G Thurman
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Infection and immunity     Volume:  69     ISSN:  0019-9567     ISO Abbreviation:  Infect. Immun.     Publication Date:  2001 Sep 
Date Detail:
Created Date:  2001-08-13     Completed Date:  2001-09-13     Revised Date:  2013-04-17    
Medline Journal Info:
Nlm Unique ID:  0246127     Medline TA:  Infect Immun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  5883-91     Citation Subset:  IM    
Affiliation:
Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina at Chapel Hill, North Carolina 27599-7365, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Ankle Joint / physiology
Arthritis, Reactive / chemically induced*,  prevention & control*
Body Weight
Calcium / metabolism
Chloride Channels / metabolism*
Dietary Supplements
Eating
Glycine / administration & dosage*,  metabolism
Ion Channel Gating
Macrophages / metabolism
Male
NF-kappa B / metabolism
Peptidoglycan / toxicity*
Polysaccharides, Bacterial / toxicity*
Rats
Rats, Inbred Lew
Spleen / cytology
Superoxides / metabolism
Grant Support
ID/Acronym/Agency:
P30 KD34987//PHS HHS
Chemical
Reg. No./Substance:
0/Chloride Channels; 0/NF-kappa B; 0/Peptidoglycan; 0/Polysaccharides, Bacterial; 11062-77-4/Superoxides; 56-40-6/Glycine; 7440-70-2/Calcium
Comments/Corrections

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


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