Advanced

Nephritogenic activity of IgA-binding streptococcus pyogenes : An experimental model of IgA glomerulonephritis

Burova, L. A.; Pigarevsky, P. V.; Snegova, V. A.; Duplik, N. V.; Schalén, Claës LU and Totolian, Artem A. (2016) In Medical Immunology (Russia) 18(3). p.221-230
Abstract

The aim of present study was to arrange an experimental rabbit model for IgA-nephropathy. To this purpose, an approach was attempted which was previously successfully applied in rabbits, aiming for induction of post-streptococcal glomerulonephritis (PSGN). To induce the nephropathy, we used two Streptococcus pyogenes strains of M4 and M60 serotypes which showed differential IgA-binding capacity mediated by the IgAFc microbial receptors. The renal tissue damage was developed in most animals treated with emm60 S. pyogenes characterized by marked IgAFcR expression and higher IgA-binding ability. By means of morphometric analysis. Significant morphological and immunochemical glomerular changes were revealed in 6/10 rabbits, as follows: (i)... (More)

The aim of present study was to arrange an experimental rabbit model for IgA-nephropathy. To this purpose, an approach was attempted which was previously successfully applied in rabbits, aiming for induction of post-streptococcal glomerulonephritis (PSGN). To induce the nephropathy, we used two Streptococcus pyogenes strains of M4 and M60 serotypes which showed differential IgA-binding capacity mediated by the IgAFc microbial receptors. The renal tissue damage was developed in most animals treated with emm60 S. pyogenes characterized by marked IgAFcR expression and higher IgA-binding ability. By means of morphometric analysis. Significant morphological and immunochemical glomerular changes were revealed in 6/10 rabbits, as follows: (i) massive IgA deposition in the mesangial glomerular cells, atrophy of the capillary net, and tissue oedema; (ii) marked C3-complement deposition in proximal and distal tubules; (iii) a significant infiltration of cortical and medullar areas by lymphocytes associated with weak TNFα production. Noteworthy, we did not observe local IgG deposition in any cases, thus allowing to exclude any role of anti-IgG, or other IgG's in evolution of the pathology. Alternatively, the IgA-deposits may occur due to microbial IgA FcR-IgAcontaining cmplexes, as earlier shown by the Swedish scientists. The above tissue changes were completely absent in kidneys of control animals. Taken together, these data suggest that we have developed an experimental model similar to IgA-nephropathy in humans. The results also extend our knowledge on pathogenic effects of the IgA Fc-binding proteins of Streptococcus pyogenes.

(Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Experimental model, IgA nephropathy, IgA-binding streptococci, Streptococcus pyogenes
in
Medical Immunology (Russia)
volume
18
issue
3
pages
10 pages
publisher
Russian Association of Allergologists and Clinical Immunologists, St. Petersburg Regional Branch (SPb RAACI)
external identifiers
  • scopus:84986907364
ISSN
1563-0625
language
Russian
LU publication?
yes
id
eb61236e-3d6e-4296-999b-382616056b31
date added to LUP
2016-10-07 11:01:05
date last changed
2017-01-20 14:22:17
@article{eb61236e-3d6e-4296-999b-382616056b31,
  abstract     = {<p>The aim of present study was to arrange an experimental rabbit model for IgA-nephropathy. To this purpose, an approach was attempted which was previously successfully applied in rabbits, aiming for induction of post-streptococcal glomerulonephritis (PSGN). To induce the nephropathy, we used two Streptococcus pyogenes strains of M4 and M60 serotypes which showed differential IgA-binding capacity mediated by the IgAFc microbial receptors. The renal tissue damage was developed in most animals treated with emm60 S. pyogenes characterized by marked IgAFcR expression and higher IgA-binding ability. By means of morphometric analysis. Significant morphological and immunochemical glomerular changes were revealed in 6/10 rabbits, as follows: (i) massive IgA deposition in the mesangial glomerular cells, atrophy of the capillary net, and tissue oedema; (ii) marked C3-complement deposition in proximal and distal tubules; (iii) a significant infiltration of cortical and medullar areas by lymphocytes associated with weak TNFα production. Noteworthy, we did not observe local IgG deposition in any cases, thus allowing to exclude any role of anti-IgG, or other IgG's in evolution of the pathology. Alternatively, the IgA-deposits may occur due to microbial IgA FcR-IgAcontaining cmplexes, as earlier shown by the Swedish scientists. The above tissue changes were completely absent in kidneys of control animals. Taken together, these data suggest that we have developed an experimental model similar to IgA-nephropathy in humans. The results also extend our knowledge on pathogenic effects of the IgA Fc-binding proteins of Streptococcus pyogenes.</p>},
  author       = {Burova, L. A. and Pigarevsky, P. V. and Snegova, V. A. and Duplik, N. V. and Schalén, Claës and Totolian, Artem A.},
  issn         = {1563-0625},
  keyword      = {Experimental model,IgA nephropathy,IgA-binding streptococci,Streptococcus pyogenes},
  language     = {rus},
  number       = {3},
  pages        = {221--230},
  publisher    = {Russian Association of Allergologists and Clinical Immunologists, St. Petersburg Regional Branch (SPb RAACI)},
  series       = {Medical Immunology (Russia)},
  title        = {Nephritogenic activity of IgA-binding streptococcus pyogenes : An experimental model of IgA glomerulonephritis},
  volume       = {18},
  year         = {2016},
}