Experimental poststreptococcal glomerulonephritis elicited by IgG Fc-binding M family proteins and blocked by IgG Fc fragment.
Burova, Larissa ; Pigarevsky, Peter ; Seliverstova, Valentina ; Gupalova, Tatiana ; Schalén, Claës LU
and Totolian, Artem
(2012)
In APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
120(3).
p.221-230
- Abstract
- Burova L, Pigarevsky P, Seliverstova V, Gupalova T, Schalén C, Totolian A. Experimental poststreptococcal glomerulonephritis elicited by IgG Fc-binding M family proteins and blocked by IgG Fc fragment. APMIS 2012; 120: 221-30. The pathogenesis of acute poststreptococcal glomerulonephritis (APSGN), a major nonsuppurative complication of group A streptococcal (GAS) throat or skin disease, remains unclear. During the years, various theories based on certain streptococcal extracellular factors, as well as immunological mimicry between streptococci and renal tissue, have been forwarded. We earlier reported that many clinical GAS isolates with documented nephritogenic capacity show non-immune binding of monomeric or aggregated IgG. Moreover, in... (More)
- Burova L, Pigarevsky P, Seliverstova V, Gupalova T, Schalén C, Totolian A. Experimental poststreptococcal glomerulonephritis elicited by IgG Fc-binding M family proteins and blocked by IgG Fc fragment. APMIS 2012; 120: 221-30. The pathogenesis of acute poststreptococcal glomerulonephritis (APSGN), a major nonsuppurative complication of group A streptococcal (GAS) throat or skin disease, remains unclear. During the years, various theories based on certain streptococcal extracellular factors, as well as immunological mimicry between streptococci and renal tissue, have been forwarded. We earlier reported that many clinical GAS isolates with documented nephritogenic capacity show non-immune binding of monomeric or aggregated IgG. Moreover, in a rabbit model of APSGN we obtained evidence for an important role of streptococcal IgG Fc binding proteins (IgGFcBPs) belonging to the M family surface proteins; thus, hyperimmunization by whole IgGFcBP-positive streptococci was shown to induce renal glomerular changes with deposition of IgG and complement C3, resembling the picture recorded in human APSGN. These typical renal changes were always preceded by the appearance of circulating anti-IgG antibodies. In the present work, using the same rabbit model, each of two purified IgGFcBPs, isolated from type M22 GAS, were found to elicit glomerular degenerative damage comparable to that caused by whole bacteria, as well as formation of anti-IgG. In addition, the induction by whole streptococci (type M1) of experimental APSGN was inhibited by the i.v. administration of purified human or rabbit IgG Fc, but not Fab, fragment, supporting the importance of Fc-mediated mechanisms in causation of glomerulonephritis. We propose that anti-IgG antibody, induced by streptococcal IgGFcBP, facilitated renal accumulation of IgG-containing complexes, which in turn triggered complement deposition and proinflammatory cascades. Further studies on the possible beneficial effect of IgG Fc fragment in APSGN should be of interest. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/2366804
- author
- Burova, Larissa
; Pigarevsky, Peter
; Seliverstova, Valentina
; Gupalova, Tatiana
; Schalén, Claës
LU
and Totolian, Artem
- organization
- publishing date
- 2012
- type
- Contribution to journal
- publication status
- published
- subject
- in
- APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
- volume
- 120
- issue
- 3
- pages
- 221 - 230
- publisher
- John Wiley & Sons Inc.
- external identifiers
-
- wos:000300447200008
- pmid:22339680
- scopus:84857120186
- pmid:22339680
- ISSN
- 1600-0463
- DOI
- 10.1111/j.1600-0463.2011.02826.x
- language
- English
- LU publication?
- yes
- id
- 9ec3ef81-92a1-4c9f-8c75-3bc8a5259811 (old id 2366804)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/22339680?dopt=Abstract
- date added to LUP
- 2016-04-04 07:06:14
- date last changed
- 2023-01-05 06:31:12
@article{9ec3ef81-92a1-4c9f-8c75-3bc8a5259811,
abstract = {{Burova L, Pigarevsky P, Seliverstova V, Gupalova T, Schalén C, Totolian A. Experimental poststreptococcal glomerulonephritis elicited by IgG Fc-binding M family proteins and blocked by IgG Fc fragment. APMIS 2012; 120: 221-30. The pathogenesis of acute poststreptococcal glomerulonephritis (APSGN), a major nonsuppurative complication of group A streptococcal (GAS) throat or skin disease, remains unclear. During the years, various theories based on certain streptococcal extracellular factors, as well as immunological mimicry between streptococci and renal tissue, have been forwarded. We earlier reported that many clinical GAS isolates with documented nephritogenic capacity show non-immune binding of monomeric or aggregated IgG. Moreover, in a rabbit model of APSGN we obtained evidence for an important role of streptococcal IgG Fc binding proteins (IgGFcBPs) belonging to the M family surface proteins; thus, hyperimmunization by whole IgGFcBP-positive streptococci was shown to induce renal glomerular changes with deposition of IgG and complement C3, resembling the picture recorded in human APSGN. These typical renal changes were always preceded by the appearance of circulating anti-IgG antibodies. In the present work, using the same rabbit model, each of two purified IgGFcBPs, isolated from type M22 GAS, were found to elicit glomerular degenerative damage comparable to that caused by whole bacteria, as well as formation of anti-IgG. In addition, the induction by whole streptococci (type M1) of experimental APSGN was inhibited by the i.v. administration of purified human or rabbit IgG Fc, but not Fab, fragment, supporting the importance of Fc-mediated mechanisms in causation of glomerulonephritis. We propose that anti-IgG antibody, induced by streptococcal IgGFcBP, facilitated renal accumulation of IgG-containing complexes, which in turn triggered complement deposition and proinflammatory cascades. Further studies on the possible beneficial effect of IgG Fc fragment in APSGN should be of interest.}},
author = {{Burova, Larissa and Pigarevsky, Peter and Seliverstova, Valentina and Gupalova, Tatiana and Schalén, Claës and Totolian, Artem}},
issn = {{1600-0463}},
language = {{eng}},
number = {{3}},
pages = {{221--230}},
publisher = {{John Wiley & Sons Inc.}},
series = {{APMIS : acta pathologica, microbiologica, et immunologica Scandinavica}},
title = {{Experimental poststreptococcal glomerulonephritis elicited by IgG Fc-binding M family proteins and blocked by IgG Fc fragment.}},
url = {{http://dx.doi.org/10.1111/j.1600-0463.2011.02826.x}},
doi = {{10.1111/j.1600-0463.2011.02826.x}},
volume = {{120}},
year = {{2012}},
}