Neuraminidase Treated Homologous IgG and Immune Deposit Renal Disease in Inbred Rats

Griswold, William R.; McIntosh, James; Weil, Richard; McIntosh, Rawle M.

doi:10.3181/00379727-148-38680

Cited by 11 publications

(5 citation statements)

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“…This streptococcal strain was isolated from a patient with poststreptococcal glomerulonephritis. In subsequent studies, these investigators found that the immunoglobulin so altered had the characteristics of a cryoglobulin and the potential for producing nephritis in experimental animals (14,22,23). Because of these findings, the present study was undertaken to determine the production of neuraminidase by group A streptococci and to characterize some of the biochemical properties of this streptococcal extracellular enzyme.…”

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confidence: 95%

Properties of extracellular neuraminidase produced by group A streptococcus

Davis¹,

Baig²,

Ayoub³

1979

Infect Immun

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Extracellular neuraminidase production by group A streptococci was examined in 92 strains. Fourteen of these strains produced appreciable amounts of enzyme; 12 of the neuraminidase-producing strains belonged to T types 1, 4, and 12. Production of the enzyme paralleled bacterial growth in culture and was maximal in medium containing 0.2% glucose. The enzyme produced by one of these strains was partially purified by ammonium sulfate fractionation and filtration on G-200 Sephadex. Its molecular weight was estimated at 90,000. Activity was optimal at pH 5.7 and in the presence of 0.01 to 0.03 M calcium and magnesium cations. The enzyme was stable at temperatures of 4 and 370C for at least 24 h but was inactivated within 10 min at temperatures of 50 and 650C. The enzyme hydrolyzed 40% of the sialic acid in bovine submaxillary mucin, but was inactive on sialyllactose, porcine submaxillary mucin, oligosaccharides derived from porcine mucin, or human orosomucoid. The Km value for this enzyme with bovine submaxillary mucin as substrate was in the order of 3.6 x 10-4 M.

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confidence: 95%

Properties of extracellular neuraminidase produced by group A streptococcus

Davis¹,

Baig²,

Ayoub³

1979

Infect Immun

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“…A rheumatoid factor found in many patients with rheumatoid arthritis is an IgM which reacts with the Fc portion of the IgG molecule (i.e., that portion for which macrophages have receptors and which is opposite the site that binds antigen). It is noteworthy that neuraminidase from the bacterium, Clostridium perfringens, can cleave sialic acid from IgG, rendering it autoimmunogenic (24). Moreover, when neuraminidase‐treated homologous IgG is administered to rats, a mild to moderate focal glomerular proliferation and basement‐membrane thickening ensues (24), caused perhaps by antigen‐autoantibody complexes.…”

Section: Possible Mechanisms Of Autoimmunitymentioning

confidence: 99%

“…It is noteworthy that neuraminidase from the bacterium, Clostridium perfringens, can cleave sialic acid from IgG, rendering it autoimmunogenic (24). Moreover, when neuraminidase‐treated homologous IgG is administered to rats, a mild to moderate focal glomerular proliferation and basement‐membrane thickening ensues (24), caused perhaps by antigen‐autoantibody complexes.…”

Section: Possible Mechanisms Of Autoimmunitymentioning

confidence: 99%

Autoimmune Disease: The Consequence of Deficient T‐Cell Function?*

Kay

1976

J American Geriatrics Society

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The age-related decrease in T-lymphocyte function is discussed in relation to the onset of autoimmune disease. It is postulated that the decrease in T-cell "immune surveillance" permits: a) the ingress of viruses whose enzymes modify host glycoproteins and render them immunogenic, and b) the replication of viruses incorporated into the genome of cells during infections in early life. The existence of immunodeficiencies too subtle to be detected by our present laboratory methods is postulated and discussed in relation to diseases observed in geriatric patients. It would seem that the prevention of some geriatric diseases should begin in the pediatrician's office.

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“…1975; Griswold et al, 1975). In this postulated mechanism, immunoglobulins are rendered autoimmunogenic by modification or interaction with streptococcal products or by incorporation into an immune complex.…”

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Acute Poststreptococcal Glomerulonephritis

Nishiyama

Kobayashi²,

Yoshizawa³

2016

Diagnostic Pathology: Kidney Diseases

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Antiglobulins were measured in the sera of 82 patients with acute poststreptococcal glomerulonephritis and correlated with Clq binding activity, serum levels of immunoglobulins and C3, site of infection, antibody titres to streptococcal enzymes, and the duration of the nephritis and interval from infection. Raised serum antiglobulins were found in 89.2 % of the patients. In addition, raised titres were detected at any time during the course of the disease and very early after streptococcal infection. The finding of antiglobulins soon after the infection suggests the possibility that they appear as a primary event in the disease. Several mechanisms have been proposed for the immune renal injury following infection with certain strains of-group A 3 haemolytic streptococcus (Zabriskie et al., 1973). Even though many morphological, clinical, and serological features strongly suggest that acute poststreptococcal glomerulonephritis (APSGN) is an immune complex disease, the precise nature of the antigen-antibody system(s) operating in the disease remains undefined (Michael et al., 1966; Lange and Treser, 1973; Zabriskie et al., 1973). The evidence suggest that antibody reacting with streptococcal antigen(s) in the circulation or locally in the glomerulus incites renal inflammatory disease (

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Neuraminidase Treated Homologous IgG and Immune Deposit Renal Disease in Inbred Rats

Cited by 11 publications

References 1 publication

Properties of extracellular neuraminidase produced by group A streptococcus

Properties of extracellular neuraminidase produced by group A streptococcus

Autoimmune Disease: The Consequence of Deficient T‐Cell Function?*

Acute Poststreptococcal Glomerulonephritis

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