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

• Published in: Clinical and experimental immunology Vol. 107; no. 1; pp. 61 - 67
• Main Authors: YOSHIZAWA, N., OSHIMA, S., TAKEUCHI, A., KONDO, S., ODA, T., SHIMIZU, J., NISHIYAMA, J., ISHIDA, A., NAKABAYASHI, I., TAZAWA, K., SAKURAI, Y.
• Format: Journal Article
• Language: English
• Published: Oxford BSL Blackwell Science Ltd 01.01.1997; Blackwell; Blackwell Science Inc
• Subjects: Acute Disease; acute glomerulonephritis; Animals; Antigens, Bacterial - toxicity; Biological and medical sciences; complement activation; experimental glomerulonephritis; Female; Glomerulonephritis; Glomerulonephritis - immunology; Glomerulonephritis - microbiology; Glomerulonephritis - pathology; Kidney Glomerulus - microbiology; Kidney Glomerulus - pathology; Kidney Glomerulus - ultrastructure; Male; Medical sciences; Nephrology. Urinary tract diseases; Nephropathies. Renovascular diseases. Renal failure; Original; preabsorbing antigen; Rabbits; streptococcal antigen; Streptococcal Infections - immunology; Streptococcal Infections - pathology; Streptococcal Infections - urine; Streptococcus; Streptococcus pyogenes - immunology; Kidney disease; Glomerulonephritis; Animal model; Urinary system disease; Pathogenesis; Acute; Rabbit; Activation; Complement; Lagomorpha; Antigen; Streptococcaceae; Vertebrata; Mammalia; Streptococcus; Animal; Bacteria; Micrococcales
• ISSN: 0009-9104; 1365-2249
• DOI: 10.1046/j.1365-2249.1997.d01-897.x

FITC‐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 γ‐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 CH50 was observed from weeks 3 to 7 (9.7 ± 0.3 U/ml at week 3; normal range 12.9 ± 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.