Partial characterization of antigenic streptococcal plasma membrane components in acute glomerulonephritis

Treser, Gerhard; Semar, M.; Ty, Antonia; Sagel, Inge; Franklin, Maxine; Lange, Kurt

doi:10.1172/jci106289

Cited by 68 publications

(34 citation statements)

References 20 publications

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“…Although antigenic sites are demonstrable in the early stages of APSGN [10][11][12] and in the glomeruli of rats injected with endostreptosin, a cytoplasmic streptococcal antigen considered to be a crude form of PA-Ag [19], we could not detect PA-Ag in the glomeruli of rabbits in our experimental model. Since circulating antibody against PA-Ag appeared in 20 of the 30 rabbits as early as 8 days after the start of immunization, the antigenic sites may have already been saturated or have suffered a steric hindrance.…”

Section: Discussionmentioning

confidence: 73%

“…Staining for rabbit -globulin and C3 was performed with commercial monospecific FITC-labelled antisera to PA-Ag and FITClabelled IgG of patients with APSGN obtained 2-3 weeks after onset. It has previously been demonstrated [10,11] antisera recognize free antigenic sites in glomeruli during the early stages of the disease. Renal specimens from the rabbits were fixed in 2 .…”

Section: Morphological Studiesmentioning

confidence: 99%

See 1 more Smart Citation

Experimental acute glomerulonephritis induced in the rabbit with a specific streptococcal antigen

Yoshizawa

Oshima²,

Takeuchi³

et al. 1997

Clinical and Experimental Immunology

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SUMMARYFITC-labelled IgG obtained from patients convalescing from acute poststreptococcal glomerulonephritis (APSGN) stains glomeruli of patients with early APSGN. We previously reported a streptococcal antigen (preabsorbing antigen (PA-Ag)) that preabsorbed the stain out of sera from the convalescent patients and thus prevented glomerular staining. To confirm the nephritogenicity of PA-Ag, we administered up to 40 mg of this antigen to rabbits for 8 days and observed them for up to 9 weeks. Immunohistological analysis showed diffuse and global glomerular staining for C3 without notable staining for°-globulin. Light microscopic examinations revealed slight to moderate proliferative glomerulonephritis with exudative change. Control rabbits, which received similar doses of bovine serum albumin, did not show significant staining for C3. A transient and significant decrease in CH 50 was observed from weeks 3 to 7 (9 . 7 6 0 . 3 U/ml at week 3; normal range 12 . 9 6 0 . 6 U/ml). This experimental model showed a resemblance to immunological and immunohistological features of APSGN in humans. Although the precise mechanisms are yet to be determined, complement activation by PA-Ag seems to hold a key position in this model and in the human disease.

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Section: Discussionmentioning

confidence: 73%

Section: Morphological Studiesmentioning

confidence: 99%

Experimental acute glomerulonephritis induced in the rabbit with a specific streptococcal antigen

Yoshizawa

Oshima²,

Takeuchi³

et al. 1997

Clinical and Experimental Immunology

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show abstract

“…PSGN is an immune complex-mediated disease (26,32) wherein the glomerular injury is probably initiated by the activity of terminal complement complex (27) and in which circulating streptococcal antigen and complement complexes are codeposited on the glomerular basement membrane early in the natural history of the disease. Antibodies to the streptococcal antigen and decreased levels of complement have also been consistently noted in PSGN patients (7).…”

Section: Discussionmentioning

confidence: 99%

Characterization of a Complement-Binding Protein, DRS, from Strains of Streptococcus pyogenes Containing the emm12 and emm55 Genes

Binks

Sriprakash

2004

Infect Immun

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An extracellular protein of Streptococcus pyogenes, streptococcal inhibitor of complement (SIC), and its variant, called DRS (distantly related to SIC), are expressed by some S. pyogenes strains. SIC from type 1 (M1) isolates of S. pyogenes interferes with complement-mediated cell lysis, reportedly via its interaction with complement proteins. In this study we demonstrate that S. pyogenes strains carrying emm12 and emm55 (the genes for the M12 and M55 proteins, respectively) express and secrete DRS. This protein, like SIC, binds to the C6 and C7 complement proteins, and competition enzyme-linked immunosorbent assay experiments demonstrate that DRS competes with SIC for C6 and C7 binding. Similarly, SIC competes with DRS for binding to the complement proteins. Despite this, the recombinant DRS preparation showed no significant effect on complement function, as determined by lysis of sensitized sheep erythrocytes. Furthermore, the presence of DRS is not inhibitory to SIC activity.

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“…Immunohistochemistry has localized a variety of different streptococcal antigens in the glomeruli of PSGN patients (Batsford et al, 2005;Michael et al, 1966;Ohkuni et al, 1983;Seegal et al, 1965;Treser et al, 1970;Villarreal et al, 1979). The foci of streptococcal infections that cause PSGN are distant from the kidney.…”

Section: Factors Involved In Psgnmentioning

confidence: 99%

Host–Pathogen Interactions in Streptococcal Immune Sequelae

Nitsche-Schmitz

Chhatwal

2012

Host-Pathogen Interactions in Streptococcal Diseases

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Partial characterization of antigenic streptococcal plasma membrane components in acute glomerulonephritis

Cited by 68 publications

References 20 publications

Experimental acute glomerulonephritis induced in the rabbit with a specific streptococcal antigen

Experimental acute glomerulonephritis induced in the rabbit with a specific streptococcal antigen

Characterization of a Complement-Binding Protein, DRS, from Strains of Streptococcus pyogenes Containing the emm12 and emm55 Genes

Host–Pathogen Interactions in Streptococcal Immune Sequelae

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