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G Andres

Publications and source records attributed to G Andres.

At least 73 records · Page 4Linked to original sources
PubMed1985

Antibody-induced redistribution of Heymann antigen on the surface of cultured glomerular visceral epithelial cells: possible role in the pathogenesis of Heymann glomerulonephritis.

In this study we analyze the ability of antibodies that produce passive Heymann glomerulonephritis to induce antigen redistribution on the surface of cultured glomerular visceral epithelial cells (GEC). Polyclonal antibodies produced by immunization with membrane vesicles prepared from proximal tubule brush borders (BB) and polyclonal (rabbit) and monoclonal (mouse) antibodies to a membrane glycoprotein (gp 330) purified from epithelial cells of rat proximal tubule were used. The study by immunofluorescence of GEC kept at 4 degrees C or fixed with paraformaldehyde showed that the three antibody preparations reacted with the plasma membrane in a punctate pattern known to be due to staining of coated pits or coated vesicles on the cell surface. At 37 degrees C and, at a slower rate, at 22 degrees C, the two polyclonal antibodies induced a rapid clustering of antigen-antibody complexes on the nonadherent surface of living cultured GEC with subsequent formation of patches and caps and, after prolonged incubation, with temporary disappearance of Heymann antigen from the cell surface, so-called antigenic modulation. Antigen redistribution and modulation were inhibited by sodium azide, indicating that these processes are energy dependent. Monovalent Fab fragments of antibodies to BB vesicles did not alter the distribution of Heymann antigen unless they were subsequently cross-linked. Monoclonal anti-gp330 induced a modest degree of antigen redistribution, which was increased by subsequent cross-linking. Exposure of glomerular epithelial cells to cytochalasin B, colchicine, or ionophore A23187 prevented or altered antigen redistribution at 37 degrees C. Furthermore, the antibody-induced antigen redistribution was associated with changes in distribution of cytoplasmic actin, myosin, and tubulin, indicating that it is related to the contractile activity GEC. LEW rats, given i.v. injection of IgG directed against BB membrane vesicles, developed passive Heymann glomerulonephritis (i.e., immune deposits in the lamina rara externa of the glomerular basement membrane). In contrast, the glomeruli of rats exposed for longer periods to larger amounts of Fab fragments of the same antibodies failed to develop immune deposits. These studies show that the antibodies to the nephritogenic antigen of Heymann glomerulonephritis may induce a redistribution of immune complexes (IC) in the membrane of glomerular epithelial cells that is similar to that produced by other plasma membrane antigen-ligand interactions.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

Hyperacute renal allograft rejection in the rabbit. The role of platelet-activating factor and of cationic proteins derived from polymorphonuclear leukocytes and from platelets.

The macroscopic signs of rejection, the levels of circulating transplantation antibodies, the histologic and immunocytochemical aspects, and the levels of platelet-activating factor (PAF) present in the venous blood were studied in two groups of rabbits that had received renal allografts, one group presensitized with multiple skin grafts and a second group unsensitized, as well as in a third group of rabbits that had received renal autografts. All of the eight allografts hyperacutely rejected by presensitized recipients had deposits of rabbit IgG, IgM, and C3 along the endothelia of the vessels and massive intravascular accumulation of platelets (Pt) as soon as 5 minutes after revascularization. PAF release was detected in 2 to 10 minutes after revascularization and was present throughout most of the 60 minutes of observation. Sixty minutes after transplantation Pt and polymorphonuclear leukocytes (PMN) obliterated the vasculature and deposits of Pt- and PMN-derived cationic proteins were detected in the lumina and in the walls of the capillaries. Similar, but less severe, findings were observed in three of six renal allografts which had transient episodes of rejection after transplantation into presensitized recipients. In contrast, circulating transplantation antibodies, macroscopic signs of rejection, vascular immune deposits, release of PAF, and microvascular thrombosis were not detected in renal allografts transplanted into unsensitized recipients or in renal autografts. The results indicate that in hyperacute renal allograft rejection there is an immediate fixation of transplantation antibodies and complement of the recipient to endothelial antigens of the graft, local release of PAF, and massive accumulation, aggregation, and degranulation of Pt and PMN in the vasculature, resulting in a binding of Pt- and PMN-derived cationic proteins to the walls of the capillaries. It is conceivable that PAF release and Pt and PMN cationic proteins may contribute, together with other lysosomal enzymes, vasoconstriction, and coagulation, to the pathogenesis of antibody- and complement-mediated hyperacute graft injury.

Animals↗
PubMed1983

Lung injury mediated by antibodies to endothelium. I. In the rabbit a repeated interaction of heterologous anti-angiotensin-converting enzyme antibodies with alveolar endothelium results in resistance to immune injury through antigenic modulation.

To study the effects of relatively long-term interaction of antibodies with surface antigens of lung endothelium, rabbits were intravenously injected for a maximum of 4 d with goat anti-rabbit lung angiotensin-converting enzyme (Gt anti-RbACE) antibodies. On day 1 69%, on day 2 13%, and on days 3 and 4 of injection none of the rabbits developed lethal pulmonary edema. By immunofluorescence microscopy, deposits of GtIgG, frequently in association with RbC3, were found along the endothelium of alveolar capillary walls in all rabbits studied on day 1, in 57% on day 2, in 33% on day 3, and in none of them on day 4. While in vitro anti-ACE antibodies bound in a linear pattern to the lung endothelium, the binding pattern in vivo was distinctly granular. The in vivo interaction of antibodies with ACE also redistributed ACE in a granular pattern along capillary walls. In contrast to the granular deposition of injected anti-ACE IgG and F(ab')2 fragments of anti-ACE IgG, Fab fragments of anti-ACE IgG localized, without fixing C3, in a linear pattern along the endothelium of lung capillaries and did not modify the normal distribution of ACE. However, when the injection of Fab fragments of Gt anti-RbACE IgG was followed by an injection of Rb anti-GtIgG serum, granular deposits of Gt Fab fragments, RbIgG and RbC3 were seen along alveolar capillary walls. Biochemical measurement of ACE activity in lung homogenates provided data in agreement with those obtained by immunofluorescence microscopy, showing diminished activity to none on day 4, with some return of ACE activity on day 5, 24 h after the last injection of antibody, and normal values on day 21. The results obtained indicate that divalent antibodies to an antigen expressed on the plasma membrane of rabbit lung endothelial cells promotes a rapid redistribution of antigenic receptors, fixation of complement and, in surviving rabbits, disappearance of the antigen from the endothelial cells that are no longer susceptible to immune injury. In vivo "immunologic enzymectomy" induced by a ligand-surface antigen interaction is an example of antigenic modulation. These events may have an important role in the pathogenesis of inflammatory lesions induced by antibodies reacting with antigens expressed on the plasma membrane of cells in the lung and in other organs.

Animals↗
PubMed1983

Release of platelet activating factor in rabbits with antibody-mediated injury of the lung: the role of leukocytes and of pulmonary endothelial cells.

This paper describes the release of platelet-activating factor (PAF) into the circulation of rabbits with acute pulmonary injury induced by antibody reacting with pulmonary endothelium. Eight rabbits were injected i.v. with 2 mg/kg of body weight of goat anti-rabbit lung angiotensin-converting enzyme gamma-globulin (GtARbACE). All animals developed acute pneumonitis, characterized by severe endothelial damage, accumulation of polymorphonuclear leukocytes (PMN) and platelets (Plt) in the lumina of alveolar capillaries, and deposits of goat IgG and rabbit C3 along alveolar capillary walls. Six of the rabbits died from acute pulmonary edema. PAF was detected in the plasma of all animals within 5 min after injection of GtARbACE. Five other rabbits were depleted of leukocytes by nitrogen mustard and then injected with 2 mg/kg of body weight of GtARbACE. In three of these rabbits release of PAF was demonstrated, though in amounts smaller than in non-leukocyte-depleted rabbits; all three animals died from pulmonary edema. After injection of 0.03 mg/kg of body weight of GtARbACE in six additional rabbits, three of them leukocyte-depleted, small amounts of PAF were detected in the circulation. None of these six rabbits died of pulmonary edema. PAF release was not observed in ten rabbits injected i.v. with 2 or 0.03 mg/kg of body weight of normal goat gamma-globulin. In separate experiments in vitro, incubation of isolated lung or thoracic aorta with GtARbACE resulted in deposits of goat IgG along endothelia and significant release of PAF. PAF was also released from endothelial cells removed from thoracic aorta by cellulose acetate paper and then incubated with GtARbACE. When segments of thoracic aorta were stripped of endothelium and then incubated with GtARbACE, PAF release could not be shown. The data obtained are consistent with the interpretation that PAF released into the circulation after binding of GtARbACE to the endothelia of lung and aorta originates from leukocytes and from lung and thoracic aorta endothelial cells.

Animals↗
PubMed1983

Splenomegaly and immune complex splenitis in rabbits with experimentally induced chronic serum sickness: immunopathological findings.

This study describes the morphological and immunocytochemical aspects of the spleen in rabbits with experimentally induced chronic serum sickness. Thirty-seven rabbits were immunized with daily injections of bovine serum albumin (BSA) and six served as non-immunized controls. The most significant lesions were found in rabbits with chronic serum sickness induced by high doses of BSA. The spleens were increased in size and in weight. Granular deposits of BSA, rabbit IgG and C3, presumably immune complexes (IC), were found in the basement membranes of the venous sinuses and of the capillaries in the marginal zone, in the walls of splenic arterioles and, occasionally, between the macrophages in the splenic cords and lymphoid cells in lymphatic follicles. An increased number of degranulated polymorphonuclear leukocytes, macrophages and giant cells, degenerative changes of dendritic cells and, in some instances, splenic fibrosis were also seen. These splenic lesions developed when the concentration of BSA-antibodies in the sera decreased. The spleens of rabbits receiving high doses of BSA in a stage between acute and chronic serum sickness were also increased in size and in weight. The red pulp was enlarged, and immune deposits were observed within macrophages but not in splenic structures. The spleens of non-responder rabbits had a slight decrease in number of lymphatic follicles and germinal centers only. The spleens of non-immunized rabbits were consistently normal. The results indicate that in rabbits receiving multiple injections of high doses of BSA, chronic serum sickness is associated with splenomegaly and IC-splenitis and that these lesions occur when the level of circulating BSA antibody declines. IC-splenitis could impair the clearance of IC and influence the immune function of the spleen. These findings could have implications in the pathogenesis of splenomegaly and of defective splenic function in human IC-mediated diseases.

Animals↗
PubMed1983

Acute lung inflammation induced in the rabbit by local instillation of 1-0-octadecyl-2-acetyl-sn-glyceryl-3-phosphorylcholine or of native platelet-activating factor.

The intratracheal instillation into rabbits of 1-0-octadecyl-2-acetyl-sn-glyceryl-3-phosphorylcholine (AGEPC) or native platelet-activating factor (PAF) was shown to induce a dose-dependent acute pulmonary inflammation characterized by accumulation of macrophages in the alveolar space, degenerative and necrotic changes of alveolar epithelium, and accumulation of polymorphonuclear leukocytes (PMNs) and platelets in the alveolar capillary lumens with degenerative changes of endothelial cells. Infiltration of alveolar septa by inflammatory cells and, in a later stage, pulmonary fibrosis were also observed. Intrabronchial instillation of lysoglyceryl ether phosphorylcholine (lyso-GEPC) produced no inflammatory changes or only mild ones. In comparison with acute inflammation induced by intratracheal instillation of C5a des Arg, which is mainly characterized by the presence of neutrophils, red blood cells, and fibrin in the alveolar space, AGEPC and native PAF seem to induce a more severe accumulation of macrophages in the alveolar space and septa and of platelet and PMNs in the lumens of alveolar capillaries. These results are compatible with the concept that during inflammatory reaction an intraalveolar release of PAF contributes to the development of pulmonary injury.

Acute Disease↗
PubMed1982

Effect of protamine on the permeability and structure of rat peritoneum.

The effect of protamine, a polycationic protein, on the mesothelial permeability and ultrastructure was evaluated in a rat model of peritoneal dialysis. The peritoneal permeability to urea and inulin were measured after the intraperitoneal instillation of protamine sulfate in varying concentrations. A functional correlation was made with the ultrastructure of omentum. Protamine concentrations between 5 and 30 micrograms/ml decreased the permeability to inulin without significantly altering that of urea. At concentrations from 30 to 75 micrograms/ml, protamine increased permeability to urea by 50% and to inulin by 20%. Mesothelial cells revealed a loss of microvilli and minor degrees of disorganization of submembranous, cytoplasmic microfilaments without significant changes in the intramembranous structure of occluding junctions. Effects were partially reversible. At a concentration of 100 micrograms/ml, there was an irreversible doubling in permeability to inulin without a comparable effect on permeability to urea associated with the disruption of occluding junctions in focal areas. This complex response to protamine suggests at least two transperitoneal diffusion pathways, transcellular and paracellular. The mesothelial cell occluding junctions may be a diffusion barrier in the latter pathway.

Animals↗
PubMed1980

Lupus band test in untreated SLE patients: correlation of immunoglobulin deposition in the skin of the extensor forearm with clinical renal disease and serological abnormalities.

This study demonstrated that 88% of untreated systemic lupus erythematosus patients with clinical renal disease displayed the deposition of immunoglobulin and complement at the dermal epidermal junction of the noninvolved light exposed extensor surface of the upper 1/3 of the forearm (P less than 0.005) (positive lupus band test). Eighty-five percent of these untreated systemic lupus erythematosus patients with anti-deoxyribonucleic acid antibodies (native and/or single stranded) (P less than 0.001) and 96% of systemic lupus erythematosus patients with hypocomplementemia had a positive lupus band test (P less than 0.001). Those systemic lupus erythematosus patients with a negative lupus band test or a positive lupus band test composed of pure IgM had a decreased incidence of renal disease, serum hypocomplementemia and anti-DNA antibodies. Their sera, however, frequently contained antibodies directed against nuclear ribonuclear protein or against the cytoplasmic non-nucleic acid glycoprotein termed Ro. On the contrary, 85% of systemic lupus erythematosus patients with a positive lupus band test composed solely or in part of IgG, had anti-DNA antibodies (P less than 0.001). Their sera also frequently contained anti-Sm antibodies. The lupus band test was found to be dynamic. In general, the appearance as well as the disappearance or the marked decrease in intensity and complexity of a positive lupus band test was found to correlate with disease exacerbation, remission and the appearance and disappearance of DNA antibodies and serum hypocomplementemia.

Antibodies, Antinuclear↗
PubMed1980

Deposition of immune complexes in ovarian follicles of mice with lupus-like syndrome.

The occurrence of immune deposits in the ovaries of mice with lupus-like syndrome was studied by immunofluorescence, light microscopy, and electron microscopy. Granular deposits of mouse IgG and C3, and occasionally gp70 and denatured DNA, were found in the zona pellucida of mature and atretic follicles. Dense deposits of foreign material were seen by light and electron microscopy in areas of ZP corresponding to the immune deposits. These lesions, presumably induced by immune complexes, resemble the "membranous" changes observed in the glomerular basement membrane in some of the same mice. Inflammatory changes of the ovarian follicles were not observed. The study of "membranous" immune complex oophoritis could contribute to the understanding of immunologic mechanisms of the female reproductive system.

Animals↗
PubMed1979

Deposition of immune complexes in the ovarian follicle of rabbits with experimental chronic serum sickness. I. Immunopathology.

In the present study, deposition of antigen-antibody complexes in the ovarian follicles of the rabbit is described. Forty-one rabbits were immunized with multiple daily injections of bovine serum albumin. Twenty-two rabbits developed systemic chronic serum sickness. The ovaries of rabbits with systemic chronic serum sickness, those of the immunized rabbits that did not develop systemic chronic serum sickness, and those of the nonimmunized rabbits were studied by light, electron, and immunofluorescence microscopy. It was found that granular deposits of bovine serum albumin, rabbit IgG, and C3, presumably as antigen-antibody complexes, were frequently present in the zona pellucida of secondary and tertiary follicles, and in the corpora atretica of rabbits with systemic chronic serum sickness. The oocytes showed an increased number of vacuoles and phagosomes containing electron-opaque material. These observations may contribute to the study of immunologic mechanisms in the pathophysiology of the female reproductive system.

Animals↗
PubMed1978

Histology of human tubulo-interstitial nephritis associated with antibodies to renal basement membranes.

Twenty-seven patients with diffuse "crescentic" glomerulonephritis (CSGN) were identified in 1,174 renal biopsies from nephritic patients. Patients were assigned to three groups on the basis of the immunofluorescent study of renal biopsy specimens and serologic findings. Group I included eight patients with antibodies to glomerular (anti-GBM) and tubular (anti-TBM) basement membranes; group II had eight patients with only anti-GBM antibodies; and group III had eleven patients with CSGN unassociated with antibodies to either GBM or TBM. Patients with anti-GBM/anti-TBM antibodies (group I) had severe tubulointerstitial (TI) nephritis, as characterized by the infiltration of polymorphonuclear leukocytes and macrophages along the TBM and peritubular vessels. In some patients, focal proliferation of epithelial cells of proximal convoluted tubules (PCT), gaps or extensive destruction of TBM, lesions in the walls of small peritubular vessels, and interstitial giant cells were also observed. Patients with anti-GBM antibodies (group II) had mild to moderate interstitial cellular infiltration and mild tubular changes. Five patients with CSGN not associated with antibodies to renal basement membranes (group III) had mild to moderate interstitial cellular infiltration and tubular changes. A sixth patient, with Wegener's disease had severe granulomatous TI lesions. The results of this study show that TI nephritis is most frequent and severe with anti-TBM antibodies are demonstrable and suggest that anti-TBM antibodies contribute to the development of TI lesions.

Adult↗
PubMed1977

Disseminated immune deposits in lupus erythematosus.

Immunohistologic studies were performed on autopsy tissues of 2 patients with systemic lupus erythematosus. All tissues examined--the kidney, lung, spleen, liver, intestine, peritoneum, and choroid plexus--contained immune deposits. Antinuclear antibody concentration in immunoglobulin G eluted from lung and spleen tissue was higher than in serum immunoglobulin G. These findings support the assumption that in systemic lupus erythematosus the renal as well as the extrarenal lesions can be attributed to vascular deposition of immune complexes.

Adolescent↗