A role of streptokinase in experimental post-streptococcal glomerulonephritis

Bürova, Larissa A.; Gavrilov, E. A.; Pigarevsky, Peter V.; Тотолян, А А

doi:10.15789/2220-7619-aro-1594

Cited by 4 publications

(2 citation statements)

References 28 publications

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“…Experiments with this GAS product were performed on mice [64,70], but it is known that Ska does not activate mouse plasminogen into plasmin, a critical step in the development of post-streptococcal glomerulonephritis. This was confirmed in our experiments (Table 1) [71]. Hence, modeling glomerulonephritis in mice may not be attributed to the disease in humans.…”

Section: Autoimmune Diseases Of Streptococcal Etiologysupporting

confidence: 85%

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Nonimmune binding of human immunoglobulins G and A by Streptococcus pyogenes: the role of this phenomenon in pathology

Burova,

Suvorov,

Pigarevsky

et al. 2023

Medical academic journal

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M and M-like proteins are key pathogenicity factors of Streptococcus pyogenes, a widely prevalent and potentially lethal bacterium. These proteins confer resistance to the hosts innate and adaptive immune response by attracting specific human proteins to the streptococcal surface. The nonimmune binding of host immunoglobulins G (IgG) and A (IgA) to M and M-like proteins via their Fc domains was first described over 50 years ago, but its role in the pathogenicity of S. pyogenes remains unclear. This discovery has had a significant impact on the development of innovative diagnostic approaches, technologies, and tools in microbiology, immunology, and molecular biology. The nonimmune binding of immunoglobulins has been suggested to play a role in immune conditions on mucosal surfaces and their secretions, but not in blood plasma, while other studies suggest it protects microbes from phagocytosis in the hosts nonimmune blood. The Fc-binding effect has been shown to increase the pathogenicity of streptococci, contributing to the development of autoimmune diseases and tissue damage in experimental animals. The experimental autoimmune process can be prevented by administering purified Fc fragments of immunoglobulins to animals. Streptococcal diseases play a significant role in the pathogenesis of IgA-nephropathy (IgAN), a mesangial proliferative process caused by initial IgA-Fc deposition in renal mesangium cells. Literature suggests a relevance of recent ideas about the important role of nonimmune Ig binding in streptococcal diseases, and further efforts are required to study the binding of Fc fragments of IgG and IgA to M and M-like proteins of S. pyogenes, with the aim of developing preventive and potentially therapeutic applications. The paper speculates on the role of nonimmune Ig binding in streptococcal diseases, including cases with various mechanisms of development. These studies also focuses on preventive and potentially therapeutic applications of Fc fragments of IgG to M or M-like proteins of S. pyogenes.

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Section: Autoimmune Diseases Of Streptococcal Etiologysupporting

confidence: 85%

“…Activation of the plasminogen of different species specificity in the presence of streptokinase C and streptokinase isolated from GAS type M1 (40/58)[71] …”

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confidence: 99%

Nonimmune binding of human immunoglobulins G and A by Streptococcus pyogenes: the role of this phenomenon in pathology

Burova,

Suvorov,

Pigarevsky

et al. 2023

Medical academic journal

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Streptococcus pyogenes: phenomenon of nonimmune binding of human immunoglobulins and its role in pathology

2022

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M and M-like proteins represent the main pathogenicity factors of Streptococcus pyogenes, a widely spread and potentially lethal bacterial pathogen. These proteins provide resistance of the microbe to innate and adaptive immune response, due to attraction of specific human proteins to the streptococcal surface. Nonimmune binding of immunoglobulins G (IgG) and A (IgA) via their Fc domains to M and M-like proteins was described over 40 years ago, but its role for the pathogenicity of Streptococcus pyogenes is far from definite resolution. The discovery of this phenomenon should be considered among quite significant achievements of modern microbiology, since it had a huge impact upon development of innovative approaches, technologies and tools for microbiological, immunological and molecular diagnostics. It also promoted fundamental studies in pathogenesis of distinct infectious states and their complications caused by S. pyogenes. The non-immune binding of host immunoglobulins was previously suggested to be important mainly in immune conditions on the surface of mucous membranes and their secretions, but not in blood plasma, whereas other studies have pointed to significance of this phenomenon in protecting microbes from phagocytosis in non-immune blood of the host. It was also shown that the effect of Fc-binding causes increased pathogenicity of streptococci both in primary focus of infection, and during chronical course of the process, thus contributing to development of autoimmune diseases caused by S. pyogenes infection and leading to tissue damage in experimental animals. The experimental autoimmune process can be prevented by administering purified Fc fragments of immunoglobulins to the animals, blocking this process at the early stages of its development. A significant place in pathogenesis of IgA nephropathy (IgAN) belongs to streptococcal diseases. IgAN has been described as a mesangial proliferative process, due to initial IgA-Fcα deposition in renal mesangium cells. The data from literature describe successful modeling of individual IgAN traits, and expand our understanding of pathogenic properties and functions of Fcα binding receptor M proteins of S. pyogenes. The data reviewed in the article also presume the relevance of recently proposed ideas about an important role of non-immune Ig binding in streptococcal diseases, even in cases that differ in their development mechanism. These studies, including possible search for tools and techniques of preventive and potentially therapeutic applications, require additional efforts to study the binding of Fc fragments of IgG and IgA to M and M-like proteins of Streptococcus pyogenes.

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Autoimmune streptococcal glomerulonephritis: the problem of nephritogenicity of Streptococcus pyogenes

Burova,

Suvorov,

Pigarevsky

et al. 2023

Russian Journal of Infection and Immunity

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Acute post-streptococcal glomerulonephritis usually occurs as a complication after a streptococcal infection due to untimely or inadequate antibiotic therapy. The etiology of post-streptococcal glomerulonephritis has been studied rather comprehensively. Today, both clinicians and microbiologists do not deny the dominant role of Streptococcus pyogenes (streptococcus attributed to serological group A, GAS). Usually, emergence of acute post-streptococcal glomerulonephritis (APSGN) is associated with the so-called GAS-related "nephritogenicity" often judged by appearance and accumulation of antibodies to the antigens and extracellular products of streptococcal cells in patient blood. This interpretation is quite loose and most likely evidence about a link to the bacterial strain, rather than its nephritogenicity. Many studies refer and still attribute a leading role of "nephritogenic" factors to various streptococcal antigens and related biologically active products. Streptococcal nephritogenic factors include cross-reacting antigens, streptokinase, cysteine proteinase, endostreptosin a GAS cell membrane protein as well as plasmin-tropic enzyme glyceraldehyde-3-phosphate dehydrogenase. Nephritogenicity of all such streptococcal products is suspected to result from the fact that they are found in renal biopsies like specific patient blood serum antibodies. Regarding a term of nephritogenicity, it has been evidenced that it cannot be attributed to any specific streptococcal cell product. This review attempted to analyze a number of bacterial products as starting factors triggering this process. APSGN can be reproduced experimentally in rabbits by intravenous administration of a heat-killed Streptococcus pyogenes culture. In our experiments, strains of serotypes 1, 4, 12, 15, 22 were used. They produced M-proteins and had the ability to bind human and rabbit immunoglobulin G by interacting with the Fc part of the IgG molecule. In numerous series of experiments, evidence was obtained regarding the initiating role of GAS IgGFc-receptor proteins in developing APSGN. Recent studies confirmed the role of streptococcal IgGFc-binding proteins in the initiation of glomerulonephritis after animals were inoculated with temperature-killed IgGFc-positive GAS. This approach excluded a large group of bacterial extracellular agents from the list of APSGN-initiating candidates. An unconventional view on the pathogenesis of GAS-infection-coupled complications may allow approaching their prevention or new treatment strategies.

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A role of streptokinase in experimental post-streptococcal glomerulonephritis

Cited by 4 publications

References 28 publications

Nonimmune binding of human immunoglobulins G and A by <i>Streptococcus pyogenes</i>: the role of this phenomenon in pathology

Nonimmune binding of human immunoglobulins G and A by <i>Streptococcus pyogenes</i>: the role of this phenomenon in pathology

Streptococcus pyogenes: phenomenon of nonimmune binding of human immunoglobulins and its role in pathology

Autoimmune streptococcal glomerulonephritis: the problem of nephritogenicity of <i>Streptococcus pyogenes</i>

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