Anti-streptococcal cell membrane and anti-human glomerular basement membrane titers in sera of patients with poststreptococcal acute glomerulonephritis and anaphylactoid purpura.

Okuhara, Kenji; Yoshimoto, Masahiro; Fujisawa, Shinichi; Watanabe, Yutaka; Okuda, Rurika

doi:10.1253/jcj.47.1293

Cited by 4 publications

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“…Многие продукты жизнедеятельности СГА изучались на предмет способности индуцировать поражение почек На роль нефритогена, претендуют перекрестно-реагирующие антигены (ПР-антигены) [31,32,78,79], стрептокиназа (Ska) [65,66,67]; цистеиновая протеиназа (SpeB) [16,30,53,60], эндострептозин -белок клеточной мембраны СГА (SCM) [48,49,70,84,91], а также поверхностный белок СГА с ферментативными свойствами -глицеральдегид-3фосфат-дегидрогеназа (GAPDH) в качестве антигена, взаимодействующий с антителами в крови лиц, переболевших АPSGN [68,69,92]. Вопрос требует тщательного анализа, поскольку перечисленные стрептококковые продукты встречаются в почечных биоптатах, а антитела к ним -в крови больных.…”

Section: антигены и биологически активные продукты Streptococcus Pyog...unclassified

“…Наличие ПР-антигенов между ними обнаруживалось с помощью моноклональных анти-SCM антител [48,49]. У пациентов с АPSGN в 71,4% случаев выявляли анти-SCM антитела, реагирующие с продуктами химического (лаурил-сульфатом) «перевара» SCM, но не с растворимой в коллагеназе мембраны гломерул; перекрестные реакции между ними отсутствовали [70]. Согласно клиническим данным высокий уровень анти-SCM антител встречается у пациентов с АPSGN, но не у лиц с неосложненной СГА-инфекцией [91].…”

Section: антигены и биологически активные продукты Streptococcus Pyog...unclassified

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

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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Section: антигены и биологически активные продукты Streptococcus Pyog...unclassified

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

Burova,

Suvorov,

Pigarevsky

et al. 2023

Russian Journal of Infection and Immunity

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“…We recently reported higher levels of antibodies to SCM antigens in the sera of children with APSGN than in those of normal controls and children with uncomplicated streptococcal pharyngitis (7,13). We produced monoclonal antibodies (MAbs) to SCM antigens (20) to identify and characterize SCM antigens associated with APSGN and examined their reactivity by the enzyme-linked immunosorbent assay (ELISA).…”

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High levels of antibodies to streptococcal cell membrane antigens specifically bound to monoclonal antibodies in acute poststreptococcal glomerulonephritis

Yoshimoto¹,

Hosoi²,

Fujisawa³

et al. 1987

J Clin Microbiol

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We produced 15 immunoglobulin G class monoclonal antibodies against antigens of the streptococcal cell membrane (SCM) of Streptococcus pyogenes (T type 12, Tanaka strain) and determined the levels in human sera of antibodies against Triton-X-extracted antigens specifically bound to each of these 15 monoclonal antibodies by enzyme-linked immunosorbent assay. Sample sera were obtained from 10 normal controls (group 1), 10 patients with streptococcal pharyngitis without sequelae (group 2), and 8 patients with acute poststreptococcal glomerulonephritis (APSGN) (group 3). Anti-streptolysin O (ASO) titers of the sera increased in the order of groups 1, 2, and 3. There was no relationship between ASO titer and the level of anti-SCM antibodies, and there was no significant difference in the level of anti-SCM antibodies determined with each of the 15 monoclonal antibodies between group 1 and group 2 sera. Group 3 sera had higher levels of antibodies to SCM antigens specifically bound to each of 14 of these 15 monoclonal antibodies than group 1 or group 2 sera did. Of these 14 monoclonal antibodies, 9 reacted with the four SCM antigens separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and electrophoretically transferred to a nitrocellulose sheet. These results suggest that high levels of antibodies to SCM antigens are related to the development of APSGN and that the systemic immune response to SCM antigens is involved in the pathogenesis of APSGN.

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Vascularites systémiques satellites d'un foyer infectieux non streptococcique

Françès

Ziza

Boisnic³

et al. 1989

La Revue de Médecine Interne

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Anti-streptococcal cell membrane and anti-human glomerular basement membrane titers in sera of patients with poststreptococcal acute glomerulonephritis and anaphylactoid purpura.

Cited by 4 publications

References 0 publications

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

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

High levels of antibodies to streptococcal cell membrane antigens specifically bound to monoclonal antibodies in acute poststreptococcal glomerulonephritis

Vascularites systémiques satellites d'un foyer infectieux non streptococcique

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