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Biomedical subjects

C Tetta

Publications and source records attributed to C Tetta.

At least 145 records · Page 8Linked to original sources
PubMed1985

Immune complexes in preeclampsia and normal pregnancy.

We determined in normal nonpregnant (group I) and normal pregnant (group II) women and in patients with preeclampsia (group III): (1) immunoglobulins and complement C3b associated with polymorphonuclear leukocytes and platelet surfaces in an attempt to evaluate the interaction in vivo of immune complexes with the membranes of these cells; (2) the occurrence of circulating immune complexes; (3) the serum levels of immunoglobulins, C3, and C4; and (4) the plasma levels of complement C3d. In patients with preeclampsia (group III), the percentages of polymorphonuclear leukocytes and platelets positive for membrane-bound IgG, IgM, IgA, and C3 were significantly higher than the percentages in groups I and II. In group III, there also was a significant increase in circulating immune complexes, as compared to groups I and II. However, circulating immune complexes were also present in significant amounts in normal pregnancy (group II). The plasma levels of complement C3d were markedly increased in the most severe cases of preeclampsia.

Adult↗
PubMed1985

Functional and molecular characterization by the CB04 monoclonal antibody of a cell surface structure exerting C3-complement receptor activity.

CB04 monoclonal antibody which reacts with an epitope of a surface molecule expressed on human monocytes has been elicited using peripheral blood lymphocytes as immunizer. The characterization of the monoclonal antibody examined at the phenotypic, molecular, and functional levels indicates that the CB04 antibody defines a structure present on monocytes, tissue macrophages, B cells, polymorphonucleates, and erythrocytes. The molecular weight (220 kD), the tissue distribution in health and disease conditions, and the involvement in relevant biological processes indicate that the CB04 structure is the receptor for the C3b fragment of the complement. The binding of the antibody to the cell surface induces inhibition of the C3bi receptorial function.

Animals↗
PubMed1985

Human platelet cationic proteins bind to rat glomeruli, induce loss of anionic charges and increase glomerular permeability.

The binding of human platelet cationic proteins (HuPlt CP) to rat renal cortex in vitro and in vivo, the loss of glomerular polyanions (GPA) and the increase in glomerular permeability were studied. HuPlt CP were purified by sequential cation-exchange chromatography and chromatofocusing, by which these proteins were shown to be highly cationic in nature (pI 10.5) and mainly composed of three molecular species of 55.60 kD, 40.45 kD, and 10 kD as studied by gel permeation in high pressure liquid chromatography and SDS-polyacrylamide gel electrophoresis. Binding of HuPlt CP to glomerular capillary walls (GCW), mesangium and to peritubular capillaries of the rat renal cortex was demonstrated by immunofluorescence, using a specific goat anti-HuPlt CP antiserum, after incubation of the sections with HuPlt CP in vitro and after injection of HuPlt CP in vivo. This interaction was ionic in nature, since treatment of sections with heparin abrogated the binding of HuPlt CP to glomerular structures. The glomerular deposits of HuPlt CP were associated with the loss of GPA as revealed by colloidal iron staining (light microscopy) in both in vitro and in vivo experiments and by ruthenium red staining (electron microscopy) in in vivo studies. After the injection of native ferritin, the increase in glomerular permeability produced by an infusion of HuPlt CP was observed by the increased ratio of counted particles within the glomerular basement membrane with respect to controls. The binding of HuPlt CP to GCW and the loss of GPA was consistent with the interpretation that HuPlt CP may increase glomerular permeability due to the neutralization of GPA.

Animals↗
PubMed1985

A possible pathogenetic role of cationic proteins (CP) released by stored granulocytes in the development of pulmonary infiltrates after granulocyte transfusions.

The cationic protein (CP) content of polymorphonuclear neutrophils (PMN) prepared for transfusion is depleted after storage. The supernatants from these PMN have in vitro a PMN aggregating activity which is abolished by the preabsorption with a specific rabbit anti-human PMN CP serum. Furthermore, when the supernatants stored for few hours were injected into New Zealand White rabbits, a marked sequestration of PMN took place in the lung microvascular bed. It is suggested that PMN storage per se can cause the release of intracellular mediators of possible pathogenetic importance in the development of the pulmonary infiltrates observed after PMN transfusions.

Adult↗
PubMed1985

The role of platelet-activating factor in experimental immune complex pathology.

Tissue localization of immune complexes (IC) after infusion of synthetic platelet-activating factor (PAF) in rabbits was studied. Bovine serum albumin (BSA) was injected intravenously either before or after the infusion of synthetic PAF, later followed by the administration of anti-BSA antibodies over a 30-min period. Control rabbits received both BSA and anti-BSA antibodies, followed by lyso-PAF or saline-BSA instead of PAF. The infusion of PAF induced structural alterations in the heart, lung and kidney which were consistent with an increased vascular permeability. Deposits of BSA, IgG, and C3 were found in the heart, lung, and kidney of rabbits infused with PAF but not in control rabbits. In the liver of PAF-infused rabbits, immune deposits were only infrequently observed, whereas they were constantly present in the cardiac valves, thoracic aorta and at the bifurcation of the renal artery as they were in the control rabbits. These results suggest that PAF favors the localization of IC in the heart, lung and kidney vessels but does not influence the formation of immune deposits at the sites of turbulence of the blood flow.

Animals↗
PubMed1985

Release of platelet-activating factor in human leukemia.

Cellular release of platelet-activating factor (PAF) was assessed in a series of human acute and chronic lymphoid and myeloid leukemias at presentation or in an active phase of the disease. PAF-like material, showing physicochemical properties similar to those of synthetic PAF and of PAF released from IgE-sensitized rabbit basophils, was found in cultures of cells from 5 of 6 acute lymphoblastic leukemias (ALL) (2 of 2 T-ALL and 3 of 4 common ALL) and from 13 of 24 B-cell chronic lymphocytic leukemias after stimulation with ionophore A23187 with or without phytohemagglutinin in the presence of acetyl coenzyme A. On the other hand, PAF was released only from 2 of 10 acute myeloblastic leukemias; both of them were of the more mature monoblastic subtype or M5 according to the French-American-British classification. Cells from all three cases of chronic myeloid leukemia studied were also capable of producing PAF. In eight cases of acute lymphoid and myeloid leukemia, the in vivo release of PAF was assessed by testing the plasma levels of this mediator. Only in two cases (one ALL and one acute myeloblastic leukemia) could detectable levels of circulating PAF be demonstrated; it is of interest that both of these cases showed clinical and hematological features of disseminated intravascular coagulation. No PAF was documented in the plasma of the five chronic leukemias tested (four B-cell chronic lymphocytic leukemias and one chronic myeloid leukemia). These findings indicate that lymphoid and myeloid leukemic cells have a different capacity of releasing PAF, possibly related to the level of cell differentiation rather than to an intrinsic property of the neoplastic cells. Furthermore, in some cases, an intravascular release of PAF may occur.

Animals↗
PubMed1985

In vivo localization of C3 on the brush border of proximal tubules of kidneys from nephrotic patients.

Deposits of C3 but not of C1q and C4 were detected on the proximal tubules of kidneys from nephrotic patients with non-selective proteinuria. The incidence of tubular C3 deposits was significantly higher in patients with membranous glomerulonephritis, focal glomerulosclerosis, membrano-proliferative glomerulonephritis and non-selective proteinuria than in patients with minimal change disease, nephrotic syndrome and selective proteinuria or in patients with glomerular disease, but without nephrotic syndrome. The occurrence of tubular C3 deposits was positively correlated with the amount of urinary C3 excretion. In vitro studies showed that the human normal kidney as well as pathologic specimens negative for in vivo tubular C3 deposits were able to bind C3 on the brush border of proximal tubules when incubated with fresh heterologous serum. In contrast, in patients with non-selective proteinuria and in vivo tubular C3 deposits, the binding of heterologous C3 to the brush border of proximal tubules was markedly reduced. The positive correlation between the occurrence of tubular C3 deposits and the urinary complement excretion, together with the detection of the C3 breakdown products in the urines further supported the hypothesis that complement components, once filtrated through the glomerular barrier, might be activated by the brush border of the proximal tubule.

Adolescent↗
PubMed1985

Direct interaction between polymorphonuclear neutrophils and cuprophan membranes in a plasma-free model of dialysis.

Plasma-free, purified, normal, human polymorphonuclear neutrophils (PMN) were recirculated for 60 minutes in an experimental model of dialysis using cuprophan membranes and acetate or bicarbonate dialysate. At different time intervals, the intracellular contents of PMN-derived cationic proteins (NCP), the release of lysosyme, beta-glucuronidase and PAF as well as the occurrence of PMN and platelet aggregating activities in the supernatants were evaluated. The formation of PMN aggregates, the depletion of intracellular contents of NCP together with the release of lysosomal constituents occurred early (5-10 min) in the course of recirculation. These events were concomitant with the occurrence of PMN aggregating activity in the supernatants due to the release of NCP, as it was antagonised (30-40%) by a rabbit anti-human NCP, and to the release of PAF which also accounted for the platelet aggregating activity that was independent from both adenosine diphosphate and cyclo-oxygenase inhibitors. These data suggest that direct interaction occurs between human PMN and cuprophan in in vitro conditions in the absence of plasma factors and point to a role for cellular mediators in the pathogenesis of the intravascular alterations occurring early in haemodialysis.

Cell Aggregation↗
PubMed1984

Platelet-activating factor-induced loss of glomerular anionic charges.

The urinary protein excretion rate, the glomerular localization of cationic proteins (CP) derived from platelets and polymorphonuclear neutrophils (PMN) and the loss of fixed anionic charges were studied in rabbits infused with synthetic 1-0-octadecyl-2-acetyl-sn-glyceryl-3-phosphorylcholine [platelet activating factor (PAF), 1.5 micrograms/kg in 2 ml of saline containing 0.25% bovine serum albumin (BSA)]. The urinary protein excretion rate, unaffected by diphenhydramine, an antihistaminic agent, reached its maximum at 180 min and decreased 24 hr after PAF infusion. The localization of CP derived from platelets and PMN was investigated by immunofluorescence using specific antisera. Platelet-derived CP were detectable in glomeruli at 15 min and, particularly, at 180 min after PAF infusion. Cells positive for CP derived from PMN accumulated within 15 min in the glomerular capillaries and, later (180 min), cytoplasmic depletion and localization in glomerular capillary walls occurred. CP deposits were associated with the loss of fixed anionic charges as detected by ruthenium red and colloidal iron staining. Rabbits infused with 1-0-octadecyl-sn-glyceryl-3-phosphorylcholine (lyso-PAF) or saline-BSA alone had none of the alterations described above. The development of proteinuria, the glomerular localization of platelet- and PMN-derived CP and the concomitant loss of fixed anionic charges suggested the possibility that, once CP were released in the circulation from PAF-stimulated platelets and PMN, they bound to, and neutralized, fixed anionic charges, resulting in enhanced glomerular permeability.

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

Inhibitory effect of prostacyclin (PGI2) on neutropenia induced by intravenous injection of platelet-activating-factor (PAF) in the rabbit.

Intravenous injection into rabbits of 1-O-octadecyl-2-acetyl-sn-glyceryl-3-phosphorylcholine (synthetic Platelet-Activating Factor (PAF)) or PAF derived from rabbit basophils caused acute thrombocytopenia and neutropenia which was consequent to the formation of intravascular polymorphonuclear neutrophil (PMN) aggregates and to their sequestration in the microvasculature, primarily of the lung. Infusion of prostacyclin (PGI2; 10 ng/Kg/min to 50 ng/Kg/min) inhibited in a dose-dependent manner PAF-induced thrombocytopenia and neutropenia as well as the sequestration of PMN in the pulmonary capillary network.

Agranulocytosis↗
PubMed1983

Platelet-activating factor-mediated contraction of rabbit lung strips: pharmacologic modulation.

Synthetic platelet-activating factor (PAF) (1-0-octadecyl-2-acetyl-sn-glyceryl-3-phosphorylcholine, AGEPC) has been shown to induce a slowly developing contraction of rabbit lung parenchymal strips in an isolated organ bath. The spasmogenic effect of AGEPC appeared to be mediated by specific receptors distinct from H1, H2, cholinergic and C5a anaphylatoxin receptors. Prior exposure to AGEPC induced specific desensitization of lung parenchymal strips. Experiments with several pharmacological agents indicated that AGEPC-induced contraction was independent from cyclooxygenase, but was blocked when phospholipase A2 and lipoxygenase were inhibited and when the Ca++ channels were antagonized. Corticosteroids exhibited an inhibitory effect specific for AGEPC. Intracellular levels of cyclic AMP or cyclic GMP seemed to have a modulatory role in AGEPC-induced contraction of rabbit lung parenchymal strips.

Acetylcholine↗
PubMed1983

The brush border of proximal tubules of normal human kidney activates the alternative pathway of the complement system in vitro.

The aim of this investigation was to study complement fixation by normal human kidney tissue. C fixation was assessed on acetone-fixed sections of frozen human kidney. In addition, C consumption following incubation of normal fresh human serum with tubular or glomerular fractions of human kidney was measured. The results are consistent with the interpretation that the brush border of proximal tubules of human kidney activates the C system via the alternative pathway. It is suggested that this activation may occur in vivo in patients with a non-selective proteinuria.

Complement Activation↗
PubMed1983

Biosynthesis and release of platelet-activating factor from human monocytes.

The aim of the present study was to investigate the pathways of platelet-activating factor (PAF) production and release from human monocytes. For this purpose, both phagocytic stimuli and stimuli induced by soluble agents were used. The phagocytic stimuli exerted their effect in a receptor-specific mechanism related to surface Fc, C3b and C3d receptors. Stimuli induced by soluble agents, such as A23187 and pH 10.6, which do not require interaction with specific receptors, were also effective in inducing PAF release. In contrast, C5a, a soluble agent which induces a receptor-mediated release of PAF from neutrophils, failed to induce PAF release from monocytes. PAF release from monocytes could be dissociated from phagocytosis and from release of lysozyme. The PAF release required the presence of extracellular cations, the activation of membrane esterase and phospholipase A2 and the integrity of the microfilament system. Moreover, PAF release was modulated by lipoxygenase and intracellular cAMP levels. The relevance of an acetylation process in the biosynthesis of PAF was suggested by the increase of PAF yields in the presence of sodium acetate and by the incorporation of 14C-sodium acetate into molecules of active PAF.

Acetates↗
PubMed1983

Effect of prostacyclin (PGI2) on immune-complex-induced neutropenia.

This study reports the results of in vitro and in vivo investigations on the effect of prostacyclin (PGI2) on polymorphonuclear neutrophils (PMN) challenged with immune complexes (IC). In vitro, PGI2 does not affect the interaction of IC with PMN membrane receptors, but prevents the ensuing PMN aggregation and secretion of platelet-activating factor, a lipid mediator responsible for immune-induced PMN aggregation. In vivo, the infusion of PGI2 in New Zealand white rabbits injected with IC prevents IC-induced neutropenia and thrombocytopenia as well as the embolization of PMN into the pulmonary peripheral capillary network. These results suggest a physiological role for PGI2 in modulating the interaction between IC and PMN.

Agranulocytosis↗