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Myocardial tissue damage in rabbits injected with group A streptococci, types M1 and M22. Role of bacterial immunoglobuhn G-binding surface proteins

Burova, LA; Nagornev, VA; Pigarevsky, PV; Gladilina, MM; Gavrilova, EA; Seliverstova, VG; Totolian, AA; Thern, A and Schalén, Claës LU (2005) In Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS) 113(1). p.21-30
Abstract
Acute rheumatic fever (ARF) and acute poststreptococcal glomerulonephritis (APSGN), two important sequelae of streptococcal throat or skin infections, according to current concepts may be elicited by autoimmune mechanisms due to molecular mimicry between group A streptococci (GAS) and human tissue. In the case of APSGN, however, Our experimental data have indicated that GAS immunoglobulin-binding surface proteins (IgG Bps) might be of pathogenic significance by triggering anti-IgG production and immune complex formation leading to renal damage. Thus, rabbits injected with IEG-binding, as opposed to non-binding, GAS strains were found to develop renal deposition of IgG and complement factor C3 and inflammatory and degenerative glomerular... (More)
Acute rheumatic fever (ARF) and acute poststreptococcal glomerulonephritis (APSGN), two important sequelae of streptococcal throat or skin infections, according to current concepts may be elicited by autoimmune mechanisms due to molecular mimicry between group A streptococci (GAS) and human tissue. In the case of APSGN, however, Our experimental data have indicated that GAS immunoglobulin-binding surface proteins (IgG Bps) might be of pathogenic significance by triggering anti-IgG production and immune complex formation leading to renal damage. Thus, rabbits injected with IEG-binding, as opposed to non-binding, GAS strains were found to develop renal deposition of IgG and complement factor C3 and inflammatory and degenerative glomerular changes resembling the picture seen in APSGN. In the present study, cardiac tissue material from rabbits injected with GAS was investigated. After 8 or more weeks of intravenous (i.v.) injections, minimal changes were seen in those animals receiving an IgG non-binding GAS strain, type T27, whereas those animals receiving either of two IgG-binding GAS strains, types M1 or M22, developed strong inflammatory and degenerative myocardial changes accompanied by deposition of IgG and C3. Furthermore, on injecting rabbits with defined mutants of a type M22 strain, the development of myocardial tissue damage proved to be dependent on the presence of streptococcal IgG-binding activity. Our results demonstrate that myocardial tissue changes may be induced in the rabbit by i.v. injection of whole heat-killed GAS of at least two M serotypes. Conceivably, induction of immune complexes by bacterial IqG BPs may lead to myocardial deposition of IgG, in turn triggering a series of events, involving the complement system and proinflammatory cytokines, with resulting tissue damage. Though many virulence factors may be involved in the development of ARF and APSGN, and a given GAS strain will never cause both, our results may suggest a new pathogenetic mechanism common to these two major non-suppurative complications. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
carditis, anti-IgG, Streptococcus pyogenes, Fc-binding protein, experimental
in
Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS)
volume
113
issue
1
pages
21 - 30
publisher
John Wiley & Sons
external identifiers
  • wos:000227103000004
  • pmid:15676011
  • scopus:14044257761
ISSN
1600-0463
DOI
10.1111/j.1600-0463.2005.apm1130104.x
language
English
LU publication?
yes
id
ab052a6b-9e09-4e0a-8fbc-97e56ed51193 (old id 253919)
date added to LUP
2007-08-17 15:25:50
date last changed
2017-01-01 05:07:24
@article{ab052a6b-9e09-4e0a-8fbc-97e56ed51193,
  abstract     = {Acute rheumatic fever (ARF) and acute poststreptococcal glomerulonephritis (APSGN), two important sequelae of streptococcal throat or skin infections, according to current concepts may be elicited by autoimmune mechanisms due to molecular mimicry between group A streptococci (GAS) and human tissue. In the case of APSGN, however, Our experimental data have indicated that GAS immunoglobulin-binding surface proteins (IgG Bps) might be of pathogenic significance by triggering anti-IgG production and immune complex formation leading to renal damage. Thus, rabbits injected with IEG-binding, as opposed to non-binding, GAS strains were found to develop renal deposition of IgG and complement factor C3 and inflammatory and degenerative glomerular changes resembling the picture seen in APSGN. In the present study, cardiac tissue material from rabbits injected with GAS was investigated. After 8 or more weeks of intravenous (i.v.) injections, minimal changes were seen in those animals receiving an IgG non-binding GAS strain, type T27, whereas those animals receiving either of two IgG-binding GAS strains, types M1 or M22, developed strong inflammatory and degenerative myocardial changes accompanied by deposition of IgG and C3. Furthermore, on injecting rabbits with defined mutants of a type M22 strain, the development of myocardial tissue damage proved to be dependent on the presence of streptococcal IgG-binding activity. Our results demonstrate that myocardial tissue changes may be induced in the rabbit by i.v. injection of whole heat-killed GAS of at least two M serotypes. Conceivably, induction of immune complexes by bacterial IqG BPs may lead to myocardial deposition of IgG, in turn triggering a series of events, involving the complement system and proinflammatory cytokines, with resulting tissue damage. Though many virulence factors may be involved in the development of ARF and APSGN, and a given GAS strain will never cause both, our results may suggest a new pathogenetic mechanism common to these two major non-suppurative complications.},
  author       = {Burova, LA and Nagornev, VA and Pigarevsky, PV and Gladilina, MM and Gavrilova, EA and Seliverstova, VG and Totolian, AA and Thern, A and Schalén, Claës},
  issn         = {1600-0463},
  keyword      = {carditis,anti-IgG,Streptococcus pyogenes,Fc-binding protein,experimental},
  language     = {eng},
  number       = {1},
  pages        = {21--30},
  publisher    = {John Wiley & Sons},
  series       = {Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS)},
  title        = {Myocardial tissue damage in rabbits injected with group A streptococci, types M1 and M22. Role of bacterial immunoglobuhn G-binding surface proteins},
  url          = {http://dx.doi.org/10.1111/j.1600-0463.2005.apm1130104.x},
  volume       = {113},
  year         = {2005},
}