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T Bricio

Publications and source records attributed to T Bricio.

15 recordsLinked to original sources
PubMed1996

Soluble adhesion molecules in renal transplantation.

Serum levels of sICAM-1 and sVCAM-1 adhesion molecules as well as TNF cytokine were measured in 50 kidney transplant recipients [14 patients with stable graft function, 18 patients with acute rejection, 10 patients with CsA toxicity, 6 patients with ATN, and 2 patients with cytomegalovirus (CMV) disease] during the first 3 postoperative weeks. All the patients studied showed, on the first posttransplant day, elevated serum levels of sICAM-1 (260 +/- 53 ng/mL). Interestingly, all the patients with good graft function presented thereafter a reduction of sICAM-1 serum levels close to the normal values (185.2 +/- 40 ng/mL). In contrast, the group of patients with acute allograft rejection showed significantly increased serum levels of sICAM-1 (371.5 +/- 86 ng/mL; p < 0.001), 3-4 days before diagnosis of acute rejection. Although sVCAM-1 levels were increased in both acute graft rejection (2263 +/- 106) and CsA toxicity (1650 +/- 315) patients, such increase was not significant among either group of patients when the group with CsA toxicity was compared with either ATN (1320 +/- 204) or stable renal function (1089 +/- 167). No statistical differences in the levels of TNF were demonstrated between the different groups of patients studied. Our findings demonstrate that quantitative determination of serum sICAM-1 may be of predictive clinical value in transplanted patients with acute renal allograft rejection.

Cyclosporine↗
PubMed1995

Passive dual immunization against tumour necrosis factor-alpha (TNF-alpha) and IL-1 beta maximally ameliorates acute aminonucleoside nephrosis.

Rats receiving a single dose (10 mg/100 g) of aminonucleoside of puromycin (PAN) develop heavy proteinuria and acute interstitial nephritis (AIN). Whole isolated glomeruli from rats injected with PAN secreted both TNF-alpha and IL-1 beta cytokines. TNF-alpha secretion was first and maximally detected on day 3, whereas IL-beta activity was found on day 7, when rats were heavily proteinuric and AIN developed. In vivo treatment with either anti-TNF-alpha or anti-IL-1 beta antibodies produced a drastic and simultaneous reduction in both levels of proteinuria and intensity of interstitial cell infiltrate. These effects improved when both antibodies were administered together. Our studies demonstrate the effectiveness of immunosuppressive therapy against these two cytokines in rats with PAN-induced nephrosis.

Animals↗
PubMed1994

Prevention of mercuric chloride-induced nephritis in the brown Norway rat by treatment with antibodies against the alpha 4 integrin.

HgCl2 induces the synthesis of anti-GBM Abs with the development of glomerular and interstitial nephritis, as well as proteinuria, in the Brown Norway rat. The development of this autoimmune disease is a consequence of the appearance of an autoreactive T cell subset-inducing activation of B cells. The administration to mercury-treated rats of the mouse anti-human VLA alpha 4 HP2/1 mAb, which cross-reacts with the rat homologue integrin, completely abrogated the interstitial cell infiltrates. As demonstrated by peripheral blood analysis, this effect is not a result of the depletion of circulating leukocytes or leukocyte subsets. Interestingly, the administration of Abs specific for the alpha 4 integrin also highly reduced anti-GBM Ab synthesis, thus preventing detectable glomerular deposits and proteinuria. Our results confirm that in vivo alpha 4 functions in adhesive interaction of circulating leukocytes and vascular endothelium, and is centrally important in the extravasation and migration of T lymphocytes to sites of tissue injury. We also found a complete absence of interstitial cell infiltrates, together with a positive glomerular IgG lineal deposition pattern, when anti-GBM Abs were passively transferred to rats pretreated with anti-alpha 4 mAb, thus indicating an independent role of alpha 4 integrin in both extravasation of immune cells and production of autoantibodies. Furthermore, these in vivo findings provide preliminary evidence for the participation of the VLA-4 integrin in mediating the intercellular interaction of leukocytes regulating the production of Abs, most likely through the existence of additional yet unknown ligand(s).

Animals↗
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↗
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

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↗
PubMed1991

Natural killer function in the rat with interstitial nephritis.

Brown Norway (BN) rats with tubulointerstitial nephritis (TIN) have an augmented NK activity. Immunological manifestations of the disease indicate the existence of a highly activated B-cell system, as reflected in the high levels of circulating antibodies and in the predominant spontaneous IgG-producing B-cells in cultures. In addition, NK cells appear to induce positive signals for antibody production either when co-cultured with B-cells alone or after treatment with poly I:C. Our results suggest that NK cells might play a role in the immunoregulation of the humoral response in this disease.

Animals↗
PubMed1989

Interstitial mononuclear cell infiltrates in experimental nephrosis: effect of PAF antagonist.

Rats receiving a single injection of either aminonucleoside of puromycin (PAN, 10 mg/100 g) or Adriamycin (ADR, 7.5 mg/kg) develop heavy proteinuria and tubulointerstitial nephritis. Interstitial mononuclear cells were markedly more intense in PAN- than in ADR-treated rats. The composition of cell infiltrates was characterised in frozen kidney sections using an immunoperoxidase staining method and a panel of specific monoclonal antibodies. The severe mixed cellular lesions observed in the PAN model on day 14 were dominated by ED1+ macrophages, OX6+ Ia-interstitial and OX8+ T-cytotoxic/suppressor cell surface markers. A similar but more discrete ADR-interstitial cell accumulation was observed on day 11 of the experiment. A correlation existed in the PAN model between the severity of interstitial nephritis and the degree of proteinuria. In contrast, there was no such correlation in ADR nephrosis. Administration of PAF antagonist (BN 52021), started on the first day and continued throughout the 4 weeks of the experiment, induced in both ADR and PAN-treated rats a partial reduction in the number of interstitial cell infiltrates. Glomeruli from normal control rats incubated with 3H acetate, substrate for lyso-PAF: acetyl-CoA acetyltransferase and ADR stimulated PAF generation. Although the precise mechanism of interstitial cell accumulation in these two models of nephrosis are still unknown, our results suggest that PAF could be an important factor involved in interstitial cell recruitment.

Acetates↗
PubMed1987

Effect of cyclosporin A on autoimmune tubulointerstitial nephritis in the brown Norway rat.

The effect of cyclosporin A (CyA) on the development of tubulointerstitial nephritis (TIN) in the brown Norway (BN) rat was assessed. All manifestations of TIN were prevented in rats by subcutaneously injected CyA (20 mg/kg/day). A short 7-day course of CyA beginning the day before immunization suppressed the primary and ongoing antibody response. In addition, delayed CyA treatment (starting on day 10 after immunization), when antibody response was established, drastically reduced the levels of serum anti-TBM IgG, and abrogated the interstitial inflammatory cell response, in spite of persistent kidney-bound TBM antibodies. These results indicate that CyA has a therapeutic effect on the BN rat model of TIN.

Animals↗