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C Sapin

Publications and source records attributed to C Sapin.

At least 55 records · Page 3Linked to original sources
PubMed1987

Neonatal IgE injections do not modify Nippostrongylus brasiliensis-induced and mercuric chloride-induced IgE increase in the rat.

The effect of neonatal IgE injections on total IgE responses was studied in two rat models. After Nippostrongylus brasiliensis infection, no differences in serum IgE level and surface or cytoplasmic IgE expression were observed between IgE-treated and control LOU/C rats. Likewise, after HgCl2 injection, IgE-treated Brown-Norway rats and controls showed no difference in serum IgE level or in the development of autoimmune glomerulonephritis and proteinuria. It has been concluded that IgE-class-restricted tolerance, induced by neonatal injections of IgE, cannot be observed in rats after strong IgE stimulation.

Animals↗
PubMed1986

Autoreactive T cells in mercury-induced autoimmune disease: in vitro demonstration.

Mercuric chloride induces in Brown-Norway rats an autoimmune disease due to a T dependent polyclonal activation of B cells. Various autoantibodies and a striking increase in total serum IgE level are observed as consequences of this polyclonal activation. The aim of this study was to investigate the in vitro response of autologous syngeneic normal lymphocytes to lymphocytes exposed in vivo or in vitro to HgCL2. Helper/inducer T cells (W3/25 +) exposed to HgCl2 were found to stimulate normal T lymphocytes in the presence of normal Ia (+) cells. The proliferating T cells also had the helper/inducer phenotype. To demonstrate the potential relevance of this in vitro phenomenon to the autoimmune disease, HgCl2-pretreated T cells were injected into the footpads of normal syngeneic recipients. Draining popliteal lymph nodes contained a highly significant number of both surface IgE positive and IgE containing cells. These experiments demonstrate that HgCl2 induces autoreactive T cells and suggest that these cells may be responsible for the autoimmune disease.

Animals↗
PubMed1986

Effect of prostaglandin E1 in brown Norway rats with mercury-induced autoimmune disease.

The effect of prostaglandin E1 on mercury-induced autoimmune disease in brown Norway rats has been investigated. Daily doses of 6 to 24 micrograms prolonged survival and significantly decreased proteinuria, deposition of immune reactants in the glomeruli, circulating anti-glomerular membrane antibody production, total serum IgE, and circulating immune complex level. A dose of 3 micrograms was also effective but to a lesser degree. These results show the efficiency of prostaglandin E1 in yet another autoimmune disease, show that the beneficial effect of prostaglandin E1 in this model is related to its immunosuppressive effects, and suggest that modification of prostaglandin-mediated suppression induced by HgCl2 might play a role in the pathogenesis of this autoimmune disease.

Alprostadil↗
PubMed1985

In vivo self-reactivity of mononuclear cells to T cells and macrophages exposed to HgCl2.

Mercuric chloride induces in Brown-Norway rats a polyclonal activation of B cells resulting in a lymphoproliferation and in the production of autoantibodies. Experiments were performed to test the role of cells modified by HgCl2 in the induction of B cell proliferation by using the popliteal lymph node assay. Spleen cells, T cells and peritoneal macrophages exposed in vivo or in vitro to HgCl2 induced a proliferation of T and B cells in the draining popliteal lymph node. Spleen cells from Lewis rats who received HgCl2 were ineffective. These data suggest that modified cells could trigger autologous lymphocyte subsets and be responsible for autoimmunity induced by HgCl2.

Animals↗
PubMed1984

Involvement of hemostasis during an autoimmune glomerulonephritis induced by mercuric chloride in brown Norway rats.

Mercuric chloride (HgCl2) induces in Brown Norway (BN) rats an autoimmune disease characterized by a biphasic glomerulonephritis (GN). A transient nephrotic syndrome occurs during the third and fourth weeks after the first HgCl2 injection. Related to nephrotic syndrome, an hypercoagulable state develops with decreased factor XII and anti-thrombin III (AT III) levels and increased factor V activity and fibrinogen concentration. Moreover, during the same period, most of the rats were found thrombocytopenic. The presence of soluble fibrin monomer complexes and of fibrin degradation products (FDP) in the plasma of these rats associated with fibrin thrombi in glomerular capillary lumen proved the occurrence of disseminated intravascular coagulation (DIC). DIC was responsible for the death of several rats but most of these survived and clotting abnormalities were no longer found. Numerous factors can explain the occurrence of DIC in this model: anti glomerular basement membrane antibodies, circulating immune complexes, complement activation and/or glomerular endothelial cell detachment. The HgCl2 induced autoimmune disease appears as a good experimental model to study the relation between coagulation process and glomerulonephritis.

Animals↗
PubMed1984

Polyclonal IgE increase after HgCl2 injections in BN and LEW rats: a genetic analysis.

An autoimmune disease and a dramatic increase in total serum IgE concentration are observed in BN rats that are chronically injected with HgCl2. In contrast, LEW rats do not develop the characteristic glomerulonephritis and are very "low IgE responders". In this study, we examined the genetic control of total serum IgE increase after HgCl2 injection in F1 and F2 hybrids, in both backcrosses between LEW and BN rats, and in LEW.1N congenic rats. Genetic analysis was performed using peak IgE concentrations expressed as log microgram/ml. A high IgE phenotype was found to be dominant. Eighty-five percent of F2 variance was due to genetic factors (VG) while only 15% of this variance was caused by environmental factors (VE). From observations in F2 hybrids and backcrosses, estimations of additive variance (VA) and dominance variance (VD) were made following three different methods. Genetic control by about four loci is demonstrated. One of these genes is RT1-linked. This gene contributes to 25% of the phenotypic difference observed between BN and LEW rats. No correlation was found between the peak total IgE level and autoimmune disease based on IgG deposition in spleen and/or kidney.

Animals↗
PubMed1982

Polyclonal effect of HgCl2 in the rat, its possible role in an experimental autoimmune disease.

Mercuric chloride induces an autoimmune glomerulonephritis in Brown-Norway (BN) but not in Lewis (LEW) rats. Injection of HGCl2 into BN rats regularly produced a transient appearance of plaque-forming cells (PFC) of anti-2,4,6-trinitrophenyl and anti-sheep red blood cell specificity and circulating anti-single-stranded DNA antibodies. Addition of HgCl2 to spleen cell cultures from BN rats induced an increase in anti-trinitrophenyl PFC and reverse PFC. This effect was no longer observed when nylon wool column-depleted or anti-Thy-1 antiserum-treated spleen cells were cultured in the presence of HgCl1. These data suggest that HgCl2 acts as a polyclonal activator on spleen cells in BN rats, but not on isolated B lymphocytes. In contrast, no effect of HgCl2 on immunoglobulin production was observed in LEW rats. Since polyclonal activation and immune-type nephritis are both seen in BN but not in LEW rats, polyclonal activation may participate in the pathogenesis of the HgCl2-induced autoimmune disease of BN rats.

Animals↗
PubMed1982

Mercuric chloride induced autoimmune disease in Brown-Norway rats: sequential search for anti-basement membrane antibodies and circulating immune complexes.

Mercuric chloride induces in the Brown-Norway rat a biphasic autoimmune disease characterized initially by linear IgG deposits along the glomerular basement membrane followed later by granular IgG deposition. In the present study, anti-glomerular basement membrane antibodies and immune complex-like material were sequentially assessed in serial serum samples. Both were transiently found at the same period. Glomerular linear IgG deposits were present on day 11 but circulating anti-glomerular basement membrane antibodies were only found later on day 16. Circulating immune complexes were first detectable on day 8 before the earliest granular IgG deposits were first observed in the spleen vessels on day 16. The disappearance of circulating anti-glomerular basement membrane antibodies and of circulating immune complexes, although HgCl2 injections were pursued, is in agreement with the self-limited character of mercuric chloride induced autoimmune disease and suggests the induction of immunosuppressive mechanisms.

Animals↗
PubMed1982

Immune complex type disease induced by HgCl2 in Brown-Norway rats: genetic control of susceptibility.

Mercuric chloride induces a biphasic autoimmune glomerulonephritis in Brown-Norway (BN) rats but not in Lewis (LEW) rats. The genetic control of susceptibility to both phases was investigated by testing the response of segregants between BN and LEW rats and of congenic LEW.1N rats. It was confirmed that susceptibility to the first phase, characterized by the appearance of anti-glomerular basement membrane antibodies, depends on several genes one of which is RT1 linked. Susceptibility to the second phase, which is an immune complex type glomerulonephritis, was found to depend on one major RT1 linked gene or cluster of genes with a role for other(s) non-RT1 linked gene(s) controlling the magnitude of the response. However, congenic LEW.1N rats were found to be resistant. This suggests that the disease gene has been lost during the strain derivation. The question of whether both phases are two different diseases or expression of the same process cannot be definitely answered; data however indicate a dissociation of both disease processes.

Animals↗
PubMed1982

Suppression of nephrotoxic serum nephritis in rats by prostaglandin E1.

The ability of specific prostaglandins to modulate the development of nephrotoxic serum nephritis (NSN) in rats has been examined. The nephrotoxicity of one intravenous injection of antibodies directed against rat glomerular basement membrane (GBM) was markedly suppressed by treatment with a stable analog of prostaglandin E1 (15-(S)-15-methyl PGE1; 15-M-PGE1). Prostaglandin E1 treatment was shown to suppress both glomerular hypercellularity and proteinuria, while the binding of specific antibody to the GBM was not altered. These studies indicate that certain prostaglandins may play an important role in the regulation of Type II immune reactions. Further investigations of the role of arachidonic acid products undoubtedly will provide valuable information regarding the modulation of tissue injury as a result of various inflammatory reactions.

Alprostadil↗
PubMed1981

Immunoenzymatic study of the protein pathway through the glomerular barrier in rat glomerulonephritides.

Circulating anti-horseradish peroxidase (HRP) IgG antibodies were used in the rat to study the glomerular leakage of proteins in glomerulonephritis (GN) induced by aminonucleoside (AN) and in glomerulonephritis induced by mercuric chloride to produce anti-glomerular basement membrane (GBM) antibodies. In ANGN, autologous albumin and fibrinogen were also detected by immunoperoxidase techniques. In both types of GN, the proteins studied were observed in the glomerular urinary space and proximal tubular cells. No channels were visible in the lamina densa. No accumulation of proteins was seen under the epithelial slits that were not closed. In ANGN, accumulation of proteins was observed in the subepithelial space where the podocytes act as a barrier (closed slits, subepithelial blind pockets, areas covered by broad sheets of cytoplasm), but no accumulation was seen in the lamina rara externa under normal or enlarged slits and areas of large epithelial cytoplasm detachment. Statistical analysis showed that in ANGN, at the time of maximal proteinuria, the number of "micropinocytotic" vesicles in the GBM-embedded part of podocytes was not increased as compared with controls. Such vesicles were not labeled. We conclude that in both types of GN, the permeability of the GBM is diffusely increased and that the plasma proteins pass into the urinary space via an extracellular pathway.

Animals↗
PubMed1981

Induction of IgE synthesis and potentiation of anti-ovalbumin IgE antibody response by HgCl2 in the rat.

The present study demonstrates that mercuric chloride (HgCl2) induces a striking increase of total serum IgE in Brown Norway (BN) rats. Values up to several milligrams of IgE per milliliter of serum were observed. No antibody specificity was demonstrated for these IgE. Mercuric chloride also potentiated a specific anti-ovalbumin IgE response when the rats were immunized with ovalbumin. The kinetics of the response to HgCl2 was different from that to an antigenic stimulus alone: total IgE increased together with the potentiated anti-ovalbumin IgE antibody response to reach maximum values about 14 days after initiation of HgCl2 injections. The potentiated IgE antibodies represented only an insignificant fraction of total IgE. All these findings were observed in BN but not in Lewis rats. These data show analogies with those reported after parasitic infection in the rat and suggest similar mechanisms of action.

Animals↗