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F Mampaso

Publications and source records attributed to F Mampaso.

At least 55 records · Page 3Linked to original sources
PubMed1994

In vitro modulation of interleukin-1 beta secretion by cultured rat doxorubicin-stimulated whole glomeruli and dissociated mesangial glomerular cells.

Doxorubicin-stimulated whole rat glomeruli and dissociated mesangial and resident glomerular macrophage cells produced the release of interleukin (IL)-1 beta cytokine. This activity increased after the addition of lipopolysaccharide (LPS) or LPS plus indomethacin to the cultures. In the presence of WEB2086 [platelet-activating factor (PAF)-acether antagonist], this activity showed a drastic reduction, without modification after sodium furegrelate (thromboxane synthetase inhibitor) was added to the cultures. Our results also demonstrate that this IL-1 beta activity is mainly produced by glomerular-resident macrophage cells. These findings support the important role by both IL-1 beta and PAF-acether mediator factors, at the cellular level, in the rat model of doxorubicin-induced nephrosis.

Animals↗
PubMed1994

Involvement of tumor necrosis factor and platelet-activating factor in the pathogenesis of experimental nephrosis in rats.

BACKGROUND: The experimental nephrosis induced in rats by adriamycin (ADR) or puromycin aminonucleoside (PA) provide a useful model to study the participation of inflammatory mediators in the pathogenesis of proteinuria. EXPERIMENTAL DESIGN: We have measured tumor necrosis factor (TNF) and platelet-activating factor (PAF) production by glomeruli of rats with nephrosis, as well as the effect of treatment with the PAF antagonist, BN52021. We have also evaluated the in vitro effects of ADR, PA, and PAF on TNF and PAF production, cell viability, and protein synthesis in glomerular mesangial cells and glomerular epithelial cells (GEC) in culture. RESULTS: In ADR nephrosis, the greatest production of PAF was on day 14, preceding maximal proteinuria, whereas the highest levels of TNF where observed on day 21 after ADR injection, the moment at which proteinuria reached maximal levels. In PA nephrosis, glomerular PAF production peaked twice (days 1 and 15), before and after maximal proteinuria (day 11), whereas TNF production peaked from days 2 to 11, and slowly declined until day 21. In both models, treatment with BN52021 induced a striking decrease in proteinuria, as well as a diminution in glomerular TNF and PAF production. Both ADR and PA induced TNF and PAF production in whole glomeruli, glomerular mesangial cells, and GEC in culture. As shown by a 51Cr release assay, ADR and PA were toxic to GEC. This effect was inhibited by PAF antagonists and by anti-TNF antibodies. Whereas TNF was moderately toxic to GEC, PAF had no effect on 51Cr release. TNF toxicity was abolished by anti-TNF antibodies and largely diminished by PAF antagonists. CONCLUSIONS: TNF and PAF may participate in the induction of GEC damage and the development of proteinuria in two experimental models of nephrosis in rats.

Animals↗
PubMed1993

Cicaprost, a prostacyclin analog, protects renal function in uninephrectomized dogs in the absence of changes in blood pressure.

Ten dogs presenting mild chronic renal failure and hypertension after 27 months of uninephrectomy, during which they received a high sodium and high protein diet, were divided in two groups (n = 5) and followed for 15 months. The same diet was maintained and one of the groups received cicaprost treatment. The animals were periodically tested for biochemical and clinical parameters, and at months 0, 3, 6, and 15, glomerular filtration rate and renal plasma flow (RPF) were measured. Renal biopsies were made after 6 months of follow-up. Control group showed a higher thickening of pre- and intraglomerular portions of arteriolar vessels and an enhancement of mesangial matrix when compared with the treated group. Cicaprost also induced a significant elevation in RPF and a significant decrease in filtration fraction. All these findings suggest that cicaprost, an oral stable prostaglandin I2 analog, could have a protective renal effect in this experimental model.

Animals↗
PubMed1993

Expression of adhesion molecules in allograft renal dysfunction. A distinct diagnostic pattern in rejection and cyclosporine nephrotoxicity.

We have studied in thirty renal biopsies (from 30 cadaver allograft patients) the expression of both LFA-1 and VLA-4 leukocyte adhesion receptors and their respective ICAM-1 and VCAM-1 endothelial cell ligands, during early allograft dysfunction (24 +/- 5 days after transplantation), reversed either by antirejection therapy (n = 14) or by reduction in CsA dose (n = 16). We have found that the levels of expression of the integrin VLA-4 and the activation signal AIM/CD69 (activation inducer molecule) on interstitial cells were significantly (P < 0.001) higher in rejection than in nephrotoxicity. A main differential expression pattern was observed for VCAM-1, the endothelial cell ligand of VLA-4. Interestingly, a strong staining pattern of the renal vascular endothelium and 35% of tubular epithelium was obtained with anti-VCAM-1 antibody in rejection, as compared with a weak reactivity in endothelium and discrete staining pattern on tubules in nephrotoxicity. On the other hand, we found that the mean percentage of infiltrating cells bearing LFA-1 molecules and the intensity of ICAM-1 (a LFA-1 ligand) expression on endothelium were closely similar in both rejection and CsA nephrotoxicity. Nevertheless, a discrete significant (P < 0.05) "de novo" expression of ICAM-1 was present on tubular cells during rejection. Our results strongly suggest that in rejection the interstitial cell infiltrate seems to be facilitated by the contribution of both LFA-1/ICAM-1 and VLA-4/VCAM-1 cell adhesion mechanisms, and also that VLA-4/VCAM-1 leukocyte interaction does not play a role in cases with CsA nephrotoxicity. Furthermore, the differential expression patterns of VLA-4 and VCAM-1 molecules found between rejection and CsA nephrotoxicity could provide valuable immunohistochemical criteria in the diagnosis of allograft dysfunction.

Adult↗
PubMed1993

Detection of Epstein-Barr genome in the lymph nodes of Hodgkin's disease.

We have used the enzymatic in situ hybridization method to investigate the presence of Epstein-Barr virus (EBV) genome in lymph node tissues from patients with Hodgkin's disease. Also, 11 patients with persistent human immuno-deficiency virus-associated generalized lymphadenopathy as well as seven autopsy cases with no Hodgkin's disease, formed part of these studies. EBV DNA-positive reaction was demonstrated in Reed-Sternberg cells and variants in seven of 16 cases and in the small accompanying lymphocyte cell population in 14 of the 16 cases. It was also found in eight of the 11 cases with persistent generalized lymphadenopathy but in none of the lymph nodes from negative selective autopsy cases. Our results indicate that the colorimetric in situ hybridization technique is useful in EBV nucleic acid detection and cell-type localization in Hodgkin's disease. Additionally, the detection of EBV genome, not only in the diagnostic cells but in the small lymphocyte cell components, could provide new insights into the potential role of this agent in the pathogenesis of Hodgkin's disease.

AIDS-Related Complex↗
PubMed1992

Long-term beneficial effects of azathioprine addition to ongoing cyclosporine-prednisone protocol in renal transplantation.

Delayed addition of azathioprine (Aza) to an ongoing cyclosporine-prednisone protocol was started 11.3 +/- 9.9 months after renal transplantation in 31 patients. Group I (n = 10) had chronic renal function deterioration due to chronic rejection, group II (n = 11) had repeated or severe acute rejection episodes and group III (n = 10) had cyclosporine (Cs) toxicity despite drug tapering. In group I, SCr had risen over the 6 months prior to Aza addition (P < 0.05), renal function declining at a rate of -0.13 +/- 0.12 SCr(-1). In the 6 months post-Aza, renal function improved at a rate of 0.05 +/- 0.07 SCr(-1), and during the entire follow-up at a rate of 0.05 +/- 0.12 SCr(-1) (P < 0.01) with stable Cs levels. In group II the decline in renal function was greater, though the rate of decline was stopped after Aza. In group III, renal function improved in eight patients. After 23 +/- 12 months of follow-up, 15 patients had improved graft function, two were stable, 12 had worsened (nine on dialysis) and two had died. Amelioration of chronic graft dysfunction can be achieved by delayed addition of Aza to Cs-prednisone-treated renal allograft patients with chronic rejection or Cs toxicity, with long-term beneficial effects in a high proportion of patients.

Azathioprine↗
PubMed1992

Presence of circulating antibodies against brush border antigens (Fx1A) in a patient with membranous nephropathy and bilateral pyeloureteral stenosis. Comparison with idiopathic membranous nephropathy.

In a patient with membranous nephropathy and bilateral pyeloureteral stenosis with hydronephrosis, we examined the possibility that an increase in the intratubular pressure could facilitate the passage of the Fx1A antigens to the circulation. Elevated serum anti-Fx1A antibodies were detected in this particular patient by ELISA on three occasions during the disease follow-up, even though he was in clinical remission. These antibodies reacted in vitro with the tubular brush border of a normal human kidney. The anti-Fx1A antibodies isolated from the patient's sera by affinity chromatography competed with the rabbit anti-Fx1A antisera binding to plates coated with human Fx1A antigen. In immunoblotting studies the isolated specific IgG antibodies from that patient reacted with a 180 kDa antigen of the human Fx1A and with less intensity with 75 kDa and 50-55 kDa polypeptides. In none of 12 patients with idiopathic membranous nephropathy could the circulating anti-Fx1A antibodies be demonstrated. On the whole, this particular case suggests that on some occasions increased intratubular pressure could cause the release of Fx1A antigens, facilitating an autologous immunocomplex nephritis. These antigens, by contrast, do not seem to play any role in most cases of membranous nephropathy in man.

Aged↗
PubMed1992

IL-1-like production in adriamycin-induced nephrotic syndrome in the rat.

Rats receiving a single dose of adriamycin (7.5 mg/kg) develop heavy proteinuria and morphological abnormalities similar to those observed in minimal change nephrotic syndrome in humans. A concomitance between enhanced I-a display by resident glomerular macrophages, IL-1-like cytokine secreted by whole isolated rat glomeruli and proteinuria was observed in adriamycin-injected rats during the experimental protocol. In addition, in vitro studies have shown that after stimulation with adriamycin or lipopolysaccharide (LPS) this cytokine is mainly produced by resident glomerular macrophages in culture. Although the precise mechanism of proteinuria in this model needs to be further studied, our results indicate that IL-1-like cytokine could be an important mediator implicated in the structural and functional disturbances occurring at the glomerular capillary wall level in adriamycin nephrosis.

Animals↗
PubMed1992

Effect of anti-interleukin-1 administration to rats with adriamycin-induced nephrosis.

Rats receiving a single dose of adriamycin (7.5 mg/kg) develop heavy proteinuria and histologic lesions similar to those found in minimal change nephrotic syndrome in humans. We found that whole isolated glomeruli from rats injected with adriamycin secreted an IL-1-like cytokine which closely resembled macrophage IL-1. Maximal IL-1-like activity was detected on day 14 of the experiment when rats were heavily proteinuric. Administration of anti-IL-1 antiserum to rats with adriamycin-induced nephrosis provoked a transient but marked reduction in the urinary protein excretion. Our results indicate that IL-1-could be an important mediator implicated in the development of proteinuria in this experimental nephropathy.

Animals↗
PubMed1992

In situ demonstration of Epstein-Barr virus in intravenous drug abusers with generalized lymphadenopathy.

We have studied by the in situ hybridization method the presence of Epstein-Barr virus (EBV) DNA genome in lymph node tissues from 11 patients with persistent generalized lymphadenopathy. Using a biotinylated EBV DNA probe, we demonstrated EBV nucleic acid in scattered germinal centre cells in eight of the 11 cases. Our results suggest that EBV is not a determinant factor in the pathogenesis of this lymphadenopathy, but support its possible implication in B cell malignant transformation in cases of AIDS-associated lymphoma.

AIDS-Related Complex↗
PubMed1992

Production of interleukin-1-like cytokine by cultured rat glomerular macrophages.

Resident glomerular macrophages from normal rats were isolated and grown through long-term cultures in order to obtain confluent cell monolayers. These cells have a secretory function as revealed by the production of a cytokine with a molecular weight similar to interleukin-1 (IL-1). The demonstration that rat glomerular macrophages secrete an IL-1-like cytokine emphasizes the role of these cells in a number of glomerular secretory functions, including some which have been commonly attributed only to mesangial contractile cells.

Animals↗