Document Detail


Successful treatment of experimental glomerulonephritis with IdeS and EndoS, IgG-degrading streptococcal enzymes.
MedLine Citation:
PMID:  20219834     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Anti-glomerular basement membrane (anti-GBM) disease often results in end-stage renal failure despite therapy with plasma exchange and immunosuppressive drugs. The newly discovered streptococcal enzymes IgG-degrading enzyme of S.pyogenes (IdeS) and endoglycosidase S (EndoS) act with remarkable specificity on circulating IgG. In this study, we investigate their ability in vivo to prevent damage mediated by kidney-bound antibodies in a mouse model of anti-GBM disease. METHODS: Anti-GBM disease was induced in mice by injection of subnephritogenic doses of rabbit anti-mouse GBM, followed a week later by injection of monoclonal mouse anti-rabbit IgG antibodies. By administrating IdeS or EndoS as fusion partners with GST between these antibody injections, we tested their ability to prevent damage by acting on kidney-bound rabbit anti-GBM. Control animals received placebo injections. RESULTS: All animals in the positive control groups developed severe albuminuria immediately after the second antibody injection (mean, 2.51 mg/24 h; range, 0.13-8.20). This was significantly diminished by EndoS (1.3 +/- 1.3 mg/24 h) and completely prevented by IdeS (0.017 +/- 0.014 mg/24 h). Immunofluorescence studies showed that IdeS treatment effectively removed the Fc fragments of the rabbit IgG. This was accompanied by a significant reduction of the deposition of the complement components C3 and C1q, and this diminished the recruitment of leukocytes to the glomeruli. CONCLUSION: IdeS degrades IgG bound to the GBM in vivo, thereby preventing renal damage in this animal model. Most likely, IdeS would degrade both circulating and kidney-bound anti-GBM in patients with Goodpasture's disease. Whether this would lead to a halt in disease progression and a better prognosis remains to be determined.
Authors:
Rui Yang; Marielle A Otten; Thomas Hellmark; Mattias Collin; Lars Björck; Ming-Hui Zhao; Mohamed R Daha; Mårten Segelmark
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-03-10
Journal Detail:
Title:  Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association     Volume:  25     ISSN:  1460-2385     ISO Abbreviation:  Nephrol. Dial. Transplant.     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-07-19     Completed Date:  2010-10-28     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8706402     Medline TA:  Nephrol Dial Transplant     Country:  England    
Other Details:
Languages:  eng     Pagination:  2479-86     Citation Subset:  IM    
Affiliation:
Renal Division, Department of Medicine, Peking University First Hospital, Beijing, China.
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MeSH Terms
Descriptor/Qualifier:
Animals
Anti-Glomerular Basement Membrane Disease / chemically induced,  drug therapy*,  pathology
Autoantibodies / adverse effects
Bacterial Proteins / therapeutic use*
Disease Models, Animal
Glycoside Hydrolases / therapeutic use*
Immunoglobulin G / blood
Kidney Glomerulus / pathology
Male
Mice
Mice, Inbred C57BL
Treatment Outcome
Chemical
Reg. No./Substance:
0/Autoantibodies; 0/Bacterial Proteins; 0/Immunoglobulin G; 0/Mac-1-like protein, Streptococcus; 0/antiglomerular basement membrane antibody; EC 3.2.1.-/Glycoside Hydrolases; EC 3.2.1.-/NDOS protein, Streptococcus pyogenes

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


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