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 APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/253919
- author
- Burova, LA
; Nagornev, VA
; Pigarevsky, PV
; Gladilina, MM
; Gavrilova, EA
; Seliverstova, VG
; Totolian, AA
; Thern, A
and Schalén, Claës
LU
- organization
- publishing date
- 2005
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- carditis, anti-IgG, Streptococcus pyogenes, Fc-binding protein, experimental
- in
- APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
- volume
- 113
- issue
- 1
- pages
- 21 - 30
- publisher
- John Wiley & Sons Inc.
- external identifiers
-
- wos:000227103000004
- pmid:15676011
- scopus:14044257761
- pmid:15676011
- 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
- 2016-04-01 12:24:53
- date last changed
- 2023-01-03 08:13:32
@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}},
keywords = {{carditis; anti-IgG; Streptococcus pyogenes; Fc-binding protein; experimental}},
language = {{eng}},
number = {{1}},
pages = {{21--30}},
publisher = {{John Wiley & Sons Inc.}},
series = {{APMIS : acta pathologica, microbiologica, et immunologica Scandinavica}},
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}},
doi = {{10.1111/j.1600-0463.2005.apm1130104.x}},
volume = {{113}},
year = {{2005}},
}