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

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.

Author(s):  
James C.S. Kim

Bovine respiratory diseases cause serious economic loses and present diagnostic difficulties due to the variety of etiologic agents, predisposing conditions, parasites, viruses, bacteria and mycoplasma, and may be multiple or complicated. Several agents which have been isolated from the abnormal lungs are still the subject of controversy and uncertainty. These include adenoviruses, rhinoviruses, syncytial viruses, herpesviruses, picornaviruses, mycoplasma, chlamydiae and Haemophilus somnus.Previously, we have studied four typical cases of bovine pneumonia obtained from the Michigan State University Veterinary Diagnostic Laboratory to elucidate this complex syndrome by electron microscopy. More recently, additional cases examined reveal electron opaque immune deposits which were demonstrable on the alveolar capillary walls, laminae of alveolar capillaries, subenthothelium and interstitium in four out of 10 cases. In other tissue collected, unlike other previous studies, bacterial organisms have been found in association with acute suppurative bronchopneumonia.


2012 ◽  
Vol 130 (3) ◽  
pp. 205-208 ◽  
Author(s):  
Ana Lúcia R. Gonçalves ◽  
Claudio V. Silva ◽  
Marlene T. Ueta ◽  
Julia M. Costa-Cruz

PEDIATRICS ◽  
1985 ◽  
Vol 75 (6) ◽  
pp. 1127-1131
Author(s):  
Ching-Yuang Lin ◽  
Hey-Chi Hsu ◽  
Han-Yang Hung

A 4-year-old boy developed nephrotic syndrome following varicella infection. Serologic studies during the early phase of the disease demonstrated a decrease in serum C3, C4, and properdin factor B. Renal biopsy revealed an acute proliferative glomerulonephritis with deposition of immunoglobulins A (IgA) and M, C3, Clq, and varicella virus antigen in the glomerulus, suggesting an immune complex deposition. Ultrastructurally, this suggested a postinfectious immune complex glomerulonephritis. These phenomena suggested that varicella virus antigen antibody complexes were deposited in the glomerulus and activated the classic and alternative pathway of complements, leading to an immune complex glomerulonephritis. During the nephrotic phase, an increase in OKT8 cells and decrease of the OKT4 cells were demonstrated. Two months later, this alteration returned to normal as the renal disease was in remission. This change of lymphocyte subsets during varicella infection may play a role in the pathogenesis of nephrotic syndrome.


1963 ◽  
Vol 13 (2) ◽  
pp. 204-210 ◽  
Author(s):  
Walter Stahl ◽  
José Oliver-González ◽  
Amina Rivera de Sala

1968 ◽  
Vol 127 (3) ◽  
pp. 507-522 ◽  
Author(s):  
P. H. Lambert ◽  
Frank J. Dixon

The development of glomerulonephritis in NZB/W mice is closely related to the formation of antinuclear, particularly anti-DNA, antibodies. The developing inflammatory glomerular lesions are characterized by the deposition of γG- and ß1C-globulins plus DNA and possibly other nuclear antigens, presumably as complexes, in a granular to lumpy pattern along the capillary walls and in the mesangia. Elution studies revealed the γG-globulin in the glomeruli to be largely γG2A-type antibody to soluble nuclear antigens. Enhancement of the antinuclear antibody response by active immunization of young NZB/W mice with DNA-methylated BSA hastens the development and increases the severity of the glomerulonephritis. Similarly, injections of soluble DNA into NZB/W mice with circulating anti-DNA antibodies but with as yet little nephritis causes rapid progression of nephritis.


1982 ◽  
Vol 28 (6) ◽  
pp. 1259-1271 ◽  
Author(s):  
S E Ritzmann ◽  
J C Daniels

Abstract Immune-complex-mediated injury is thought to play a role in diseases such as rheumatoid arthritis, systemic lupus erythematosus, serum sickness, various infectious diseases, and malignancies. With increased appreciation of the biological and pathological significance of circulating immune complexes has come efforts to develop appropriate techniques for identifying and measuring them. Common approaches exploit such phenomena as the attachment of complement components to antigen-antibody complexes, the presence of specialized receptors for immune complexes at the surface of cells, and the ability of rheumatoid factor to bind with immune complexes. This variety of assay systems for immune complexes has yielded abstruse results in numerous human pathological conditions. Unfortunately, these results seldom correlate with one another in a given disease. Thus, use of a panel of immune complex assays has been recommended. Indirect consequences of immune complex disease may still be appraised and evaluated with some confidence in clinical medicine: measurements of C3 and C4, cryoglobulins, serum viscosity, and turbidity of serum samples. Measurement of immune complexes may be useful in diagnosis, prognosis, and therapeutic monitoring, but it is the characterization of immune complexes that holds the greatest potential for better understanding of disease mechanisms.


1971 ◽  
Vol 134 (3) ◽  
pp. 65-71 ◽  
Author(s):  
Frank J. Dixon ◽  
Michael B. A. Oldstone ◽  
Giorgio Tonietti

Observations based on elution of IgG from nephritic kidneys of NZ mice and absorption of the eluted IgG with selected antigens indicate that their immune complex nephritis involves at least two kinds of antigen-antibody complexes. Antibodies reactive with nuclear antigens account for nearly half of the IgG eluted from the kidneys while antibodies reactive with Gross viral antigens make up a significant but lesser amount. Superimposed chronic viral infections affect the nephritis of NZ mice in different ways. LCM and polyoma infections hasten and intensify the antinuclear antibody responses and glomerulonephritis of these mice while LDV infection appears to protect against both antinuclear antibody formation and development of nephritis.


1981 ◽  
Author(s):  
M A Lamb ◽  
H M Reisner ◽  
H A Cooper ◽  
R H Wagner

Immunoradiometric assays (IRMA) of FVIIIR: Ag from normal and certain variant VWD plasmas have suggested possible antigenic differences in the molecules. Studies reported thus far have used antibody specific for normal FVIIIR: Ag. We have further studied this question of antigenic differences using 2 populations of antibody isolated from an antisera prepared against highly purified human FVIII. Isolated IgG was labeled with [125-I]. The population of labeled IgG “specific” for variant FVIIIR: Ag was separated by immune complex formation with a VWD plasma previously shown, by 2% agarose crossed immunoelectrophoresis, to contain only the lower molecular weight multimers of FVIIIR: Ag. The “specific” labeled IgG was obtained by low pH dissociation and subsequent G-200 chromatography. [125-I] IgG “specific” for normal FVIIIR: Ag was similarly obtained after immune complex formation with pooled normal human plasma. Liquid phase IRMAs were performed using differential precipitation with ammonium sulfate or PEG to separate antigen-antibody complexes from free antibody. Using antibody “specific” for normal FVIIIR: Ag, a lack of parallelism was noted in the dose-response curves of variant plasmas as well as a decrease in maximum antibody bound, as compared to normal. Interestingly, when this antibody was absorbed with the variant VWD plasma and the remaining antibody used in IRMAs, none was bound by either variant or normal plasma.Using antibody “specific” for variant FVIIIR: Ag, a similar lack of parallelism in dose-response curves and a decrease in maximum antibody bound were observed. Therefore rather than antigenic differences as previously implied, these results suggest that the discrepancies noted in IRMAs of variant and normal plasmas are a function of the size of the FVIIIR: Ag multimers.


1978 ◽  
Vol 23 (12) ◽  
pp. 1098-1106 ◽  
Author(s):  
Lidia Accinni ◽  
Jan R. Brentjens ◽  
Boris Albini ◽  
Elena Ossi ◽  
David W. O'Connell ◽  
...  

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