Deposition of circulating antigen-antibody complexes in the gastrointestinal tract of rabbits with chronic serum sickness

1978 ◽  
Vol 23 (12) ◽  
pp. 1098-1106 ◽  
Author(s):  
Lidia Accinni ◽  
Jan R. Brentjens ◽  
Boris Albini ◽  
Elena Ossi ◽  
David W. O'Connell ◽  
...  
Keyword(s):  
Gastrointestinal Tract ◽  
Serum Sickness ◽  
Circulating Antigen ◽  
Antigen Antibody

Extra-glomerular lesions associated with deposition of circulating antigen-antibody complexes in kidneys of rabbits with chronic serum sickness

1974 ◽  
Vol 3 (1) ◽  
pp. 112-126 ◽  
Author(s):  
Jan R. Brentjens ◽  
David W. O'Connell ◽  
Irene B. Pawlowski ◽  
Giuseppe A. Andres
Keyword(s):  
Serum Sickness ◽  
Circulating Antigen ◽  
Glomerular Lesions ◽  
Antigen Antibody

scholarly journals THE NATURE OF ANTIGEN-ANTIBODY COMPLEXES FORMED IN RABBITS DURING AN IMMUNE RESPONSE TO BOVINE SERUM ALBUMIN

1958 ◽  
Vol 107 (5) ◽  
pp. 653-663 ◽  
Author(s):  
William O. Weigle
Keyword(s):  
Immune Response ◽  
Bovine Serum Albumin ◽  
Serum Albumin ◽  
Ammonium Sulfate ◽  
Bovine Serum ◽  
Ammonium Sulfate Precipitation ◽  
Antibody Synthesis ◽  
Circulating Antigen ◽  
Antigen Antibody

The immune elimination of soluble BSA, following an intravenous injection, is accompanied by the appearance of circulating antigen-antibody complexes. The pattern of the appearance of circulating antigen-antibody complexes and the immune elimination of antigen probably depends on the amount of antigen injected, the rate of antibody synthesis, and perhaps, the quality of antibody produced. There is no relationship between the I* antigen-antibody complexes detected during the immune response in rabbits by ammonium sulfate precipitation and the material precipitated from immune sera as a result of treatment with alkali. Alkali-precipitable material present in the serum of rabbits at a time when I* antigen is also present contain at most only traces of the antigen.

scholarly journals THE MECHANISM OF ACTION OF CORTISONE IN EXPERIMENTAL HYPERSENSITIVITY

1953 ◽  
Vol 98 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Frederick G. Germuth
Keyword(s):  
Intravenous Injection ◽  
Mechanism Of Action ◽  
Antibody Production ◽  
Inhibitory Effect ◽  
Serum Sickness ◽  
Bovine Albumin ◽  
Renal Lesions ◽  
Granulomatous Lesions ◽  
Antigen Antibody ◽  
Circulating Antibody

Cortisone markedly suppressed the cardiovascular and renal lesions of serum sickness type hypersensitivity which ordinarily develop following the intravenous injection of bovine albumin. The inhibitory effect of cortisone on the allergic granulomatous lesions of the spleen was less striking; the lesions were less extensive, but the percentage of animals affected was unchanged. Cortisone in the dosage employed had no effect on the elimination of antigen following its intravenous administration or on the appearance of circulating antibody. These findings indicate that inhibition of the lesions of serum sickness by cortisone does not depend on the suppression of antibody production. Therefore, it is inferred that cortisone somehow protects the animal from the damaging effects of antigen-antibody union.

scholarly journals EXPERIMENTAL IMMUNE COMPLEX DISEASE OF THE LUNG

1974 ◽  
Vol 140 (1) ◽  
pp. 105-125 ◽  
Author(s):  
Jan R. Brentjens ◽  
David W. O'Connell ◽  
Irene B. Pawlowski ◽  
Konrad C. Hsu ◽  
Giuseppe A. Andres
Keyword(s):  
Antibody Response ◽  
Immune Complex ◽  
Interstitial Pneumonitis ◽  
Interstitial Fibrosis ◽  
Systemic Disease ◽  
Serum Sickness ◽  
Daily Injection ◽  
Antigen Antibody ◽  
Capillary Walls ◽  
Alveolar Capillary

Membranous and/or proliferative pneumonitis, similar in certain features to human interstitial pneumonitis, developed in rabbits making hyperactive antibody response to daily injections of bovine serum albumin (BSA) administered in multiple large doses sufficient to maintain the state of relative antigen-antibody equivalence. The pulmonary lesions were associated with deposition in alveolar capillary walls and interstitium of antigen, host globulin and complement, presumably in immune complexes. In some rabbits chronic interstitial pneumonitis, characterized by thickening of alveolar capillary walls, interstitial fibrosis and deposition of fibrinogen, was observed. The production of immune complex pneumonitis seems to depend on the degree of the antibody response because rabbits developing chronic serum sickness with low doses of BSA, rabbits with acute serum sickness as well as nonresponders showed no pulmonary alterations. This observation is comparable to that described by Dixon in his studies on experimental immune complex glomerulonephritis. It is conceivable that the pulmonary pathology shown here is produced by formation of larger amounts of complexes which may persist longer at critical levels in the circulation than in rabbits immunized with a single daily injection of BSA. In conclusion this study suggests: first, that experimental chronic serum sickness can be used as a model, not only for glomerulonephritis, but also for experimental systemic disease, comparable to human systemic diseases produced by circulating antigen-antibody complexes; and second, that the pathogenesis proposed here offers an alternative to using antilung basement membrane pneumonitis for the experimental approach to the study of human lung immunopathology.

scholarly journals The Role of Nephritis-Associated Plasmin Receptor (NAPlr) in Glomerulonephritis Associated with Streptococcal Infection

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Takashi Oda ◽  
Nobuyuki Yoshizawa ◽  
Kazuo Yamakami ◽  
Yutaka Sakurai ◽  
Hanako Takechi ◽  
...  
Keyword(s):  
Renal Biopsy ◽  
Streptococcal Infection ◽  
Group A Streptococcus ◽  
Plasmin Activity ◽  
Subsequent Formation ◽  
Poststreptococcal Glomerulonephritis ◽  
Circulating Antigen ◽  
Group A ◽  
Antigen Antibody

It is well known that glomerulonephritis can occur after streptococcal infection, which is classically referred to as acute poststreptococcal glomerulonephritis (APSGN). The pathogenic mechanism of APSGN has been described by so-called immune complex theory, which involves glomerular deposition of nephritogenic streptococcal antigen and subsequent formation of immune complexesin situand/or the deposition of circulating antigen-antibody complexes. However, the exact entity of the causative antigen has remained a matter of debate. We isolated a nephritogenic antigen for APSGN from the cytoplasmic fractions of group A streptococcus (GAS) depending on the affinity for IgG of APSGN patients. The amino acid and the nucleotide sequences of the isolated protein revealed to be highly identical to those of reported plasmin(ogen) receptor of GAS. Thus, we termed this antigen nephritis-associated plasmin receptor (NAPlr). Immunofluorescence staining of the renal biopsy tissues with anti-NAPlr antibody revealed glomerular NAPlr deposition in essentially all patients with early-phase APSGN. Furthermore, glomerular plasmin activity was detected byin situzymography in the distribution almost identical to NAPlr deposition in renal biopsy tissues of APSGN patients. These data suggest that NAPlr has a direct, nonimmunologic function as a plasmin receptor and may contribute to the pathogenesis of APSGN by maintaining plasmin activity.

Circulating Antigen Antibody Complexes in Scabies

Dermatology ◽  
1978 ◽  
Vol 157 (4) ◽  
pp. 221-224 ◽  
Author(s):  
D. van Neste ◽  
J. Salmon
Keyword(s):  
Circulating Antigen ◽  
Antigen Antibody

scholarly journals STUDIES ON THE LOCALIZATION OF CIRCULATING ANTIGEN-ANTIBODY COMPLEXES AND OTHER MACROMOLECULES IN VESSELS

1963 ◽  
Vol 118 (4) ◽  
pp. 489-502 ◽  
Author(s):  
Charles G. Cochrane
Keyword(s):  
Basement Membrane ◽  
Anaphylactic Shock ◽  
Vessel Wall ◽  
Polymorphonuclear Leukocytes ◽  
Blood Stream ◽  
Soluble Antigen ◽  
Short Term ◽  
Circulating Antigen ◽  
Vessel Walls ◽  
Antigen Antibody

A short term model in which circulating antigen-antibody complexes and host complement localized in vessel walls of guinea pigs was analyzed. Localization was accomplished by subjecting the animals to anaphylactic shock. The circulating macromolecules, such as antigen-antibody complexes, appeared to localize by being trapped in the vessel wall along the basement membrane that acted as a filter during a state of increased permeability of the vessel. It was suggested that this point of localization between the endothelial cell and the basement membrane may well represent the earliest focus of inflammation in diseases caused by the deposition of injurious macromolecules such as soluble antigen-antibody complexes from the blood stream. Complexes localized in the vessel walls did not provoke Arthus-type vasculonecrotic reactions even though in both these vessels and in cutaneous Arthus reactions antibody, antigen, and host complement (C'3c) were deposited in the vessel walls. The possibility was presented that since circulating macromolecules and probably complexes deposited in (a) relatively small amounts, and (b) in a position beneath endothelial cells, they were not strongly chemotactic toward circulating polymorphonuclear leukocytes. Vasculonecrotic reactions, therefore, were not observed. It was brought out that this may be similar to the situation in glomerulonephritis induced by localized immune complexes, in which severe necrosis is not observed. In the Arthus vascular reaction, host complement was found microscopically accumulated with the immune reactants in affected vessel walls.

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