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Biomedical subjects

A Salerno

Publications and source records attributed to A Salerno.

At least 109 records · Page 6Linked to original sources
PubMed1989

Enhancement of macrophage IL-1 production by Leishmania major infection in vitro and its inhibition by IFN-gamma.

Peritoneal cells from highly susceptible BALB/c mice were infected with Leishmania major and cultured for various times in vitro. The culture supernatants contained significant levels of IL-1 which were consistently higher than those in the cell cultures stimulated with an optimal concentration of LPS. This finding extends to a macrophage cell line, P388D1, and peritoneal exudate cells stimulated with starch in vivo. However, the level of IL-1 produced was significantly reduced when the cells were preincubated with a lymphokine preparation (supernatant of Con A-stimulated rat spleen cells). The level of IL-1 produced seems to be directly correlated with the degree of parasitization of the macrophages. A similar and dose-dependent reduction in IL-1 production by infected macrophages could also be obtained when the cells were preincubated with IFN-gamma. This finding is in direct contrast to that of visceral leishmaniasis in which peritoneal macrophages from BALB/c mice infected with Leishmania donovani not only fail to produce IL-1 but also lose the capacity to produce IL-1. This apparent discrepancy is discussed in terms of a possible difference in the induction of cell-mediated immunity between the two leishmanial diseases.

Animals↗
PubMed1989

Role of the fourth complement component (C4) in the regulation of contact sensitivity. II. Qualitative differences between C4 molecules from high- and low-C4 mouse strains.

Lymph node cells collected from CBA/J mice 4 days after painting with picryl chloride induce contact sensitivity in naive recipient mice by virtue of hapten IgM immuno complexes. The immunizing capacity of these cells ("4-day" cells) is abolished after incubation of the cells with a C4-deficient guinea pig serum reconstituted with plasma or purified C4 from mice with high C4 levels (C4h), but not with plasma or purified C4 from mice with low C4 levels (C41). The inhibition of the immunizing capacity of 4-day cells is due to the activation of the early components of the classical complement pathway which is likely to result in the solubilization of membrane-bound immunocomplexes. However, the same amounts of CBA/J and BALB/c C4 have a different effect in inhibiting the induction of contact sensitivity by 4-day cells. In fact, by dose-response experiments, we have found that the amount of C41 able to inhibit the induction of contact sensitivity is about threefold higher than that of C4h. Analysis of the covalent binding ability of C4h and C41 reveals that C4h is able to bind to the surface of 4-day cells more efficiently than C41 and this probably accounts for the difference of the two C4 molecules in inhibiting the immunizing capacity of 4-day cells. Results are discussed in terms of different reactivities of C4h and C41 with the surface of 4-day cells.

Animals↗
PubMed1989

The molecular basis of the low hemolytic activity of C4 molecules from low-C4 mice with IgM-coated erythrocytes.

This study investigated the origin of the different hemolytic activity of two allotypes of murine C4, C4H (C4-high) and C4L (C4-low) in the presence of IgM-coated erythrocytes. C4H displayed a threefold higher hemolytic titer (expressed in hemolytic units/microgram protein) than C4L. No difference was found between c4H and C4L either in stability at 37 degrees C at different pH values and in the rate of C4H and C4L hydrolysis by activated Cl. The major functional difference was found in the covalent binding capacity to IgM-coated erythrocytes, with the amount of C4H bound being about threefold higher than that of C4L. A marked difference in the reactivity of the C4b fragment of C4H and C4L toward amino and hydroxyl groups was detected. Using glycine and glucose to competitively inhibit the binding of C4H and C4L, it was observed that C4L selects preferentially for the amino groups of glycine, whereas C4H reacted preferentially with the hydroxyl groups of glucose. Furthermore, the chemical modification of the red cells amino groups by ethylacetimidate, had no appreciable effect on the binding of C4H, but reduced that of C4L. Southern blot hybridization experiments using Hind III-digested liver DNA and a cDNA probe derived from the 5' end of the mRNA (clone pAT-A) indicated that the C4H allele was associated with a 5-kb Hind III fragment, whereas the C4L allele was associated with a 15-kb Hind III fragment. The possibility that a structural difference between C4H and C4L is responsible for their different reactivities is discussed.

Alleles↗
PubMed1989

Are lipid abnormalities reliable cardiovascular risk factors in dialysis patients?

Patients on chronic hemodialysis often present both hyperlipidemia and a high incidence of cardiovascular disease (CVD). Uremic hyperlipidemia has usually been regarded as one of the most important cardiovascular risk factors (CVRF) in these patients. In order to study whether the "uremia-induced" lipid abnormalities are actually associated with evidence of uremic CVD, and consequently may be considered reliable CVRF, 123 patients on chronic dialysis were reviewed for the presence of CVD and, at the same time, examined for their lipoprotein pattern and other clinical and biochemical variables. Lipids and lipoproteins did not prove helpful in our study in identifying patients with CVD. Despite the fact that they had been on dialysis for a shorter time, CVD patients were significantly older and had higher blood pressure than patients without CVD. Our data suggest that the uremia-induced lipid abnormalities are not reliable markers of CVD in dialysis patients, and support the hypothesis that dialysis per se does not accelerate the atherosclerotic process in uremic patients.

Aged↗
PubMed1988

Suppression of IL-2 production by cryopreserved peripheral blood mononuclear cells from patients with active visceral leishmaniasis in Sicily.

The ability of PBMC from eight patients with confirmed visceral leishmaniasis (Leishmania donovani) to produce IL-2 in response to PHA in vitro was investigated. PBMC from the patients produced significantly lower levels of IL-2 and had reduced proliferative response to PHA at the time of disease diagnosis compared with healthy controls. Their ability to produce IL-1 in response to LPS was, however, unaltered. The patients also showed normal levels of OKT4+ and IL-2R+ cells in the peripheral blood, as judged by specific immunofluorescence staining. All patients were given antimony therapy, and five were cured. The recovered patients showed significant improvement in the IL-2 producing capacity of their PBMC. The PBMC preparations of patients and controls were cryopreserved before and after successful chemotherapy on the patients. The frozen cell preparations were thawed and viable autologous cells cocultured with equal numbers of PBMC from patients before and after chemotherapy. The frozen cells from five healthy controls showed little or no difference whether they were cultured together or separately. In contrast, coculturing of cells from the five recovered patients with autologous pretreatment cells produced significantly and consistently lower levels of IL-2 compared with those produced when the cells were cultured separately. These results therefore demonstrate that the PBMC from patients with visceral leishmaniasis contain a population of cells that are capable of suppressing the IL-2 production by autologous PBMC from recovered patients. The method of cryopreservation should be useful for studying the immune regulation in this and other clinical diseases in vitro.

Adult↗
PubMed1988

Role of macrophages in bypassing the inhibitory activity of Newcastle disease virus on the T-suppressor-cell circuit which regulates contact sensitivity to picryl chloride.

The interaction between the paramyxovirus of Newcastle disease virus (NDV) and the T-suppressor-cell circuit which regulates the expression phase of contact sensitivity reaction to picryl chloride was investigated. NDV infection impairs the T-acceptor-cell (Tacc) activity, as demonstrated by the failure of Tacc from mice infected with NDV both on Day 0 and on Day 3 to release the nonspecific inhibitor of the passive transfer of contact sensitivity. Tacc from NDV-infected mice fail to bind appreciable amounts of exogenous T suppressor factor, so indicating that the virus eliminates this T-cell population. However, macrophages from mice infected with NDV are able to release a nonspecific inhibitor of the passive transfer of contact sensitivity, indicating that the inhibition of Tacc activity in mice infected with NDV is bypassed by macrophages, so that the T-suppressor circuit is functionally active in NDV-infected mice. The mechanism of the selective inhibition of the Tacc activity by NDV is discussed.

Animals↗
PubMed1988

Renal involvement in IgD myeloma.

Nine patients affected from IgD myeloma were studied retrospectively in order to elucidate the incidence and peculiar traits of related nephropathy. Eight patients developed chronic renal failure, and as many as 5 were already suffering from renal failure since first admission to the hospital. In 3 cases acute renal failure was the major presenting symptom of the disease. Five patients underwent a regular dialytic treatment. We suggest that the high incidence of renal involvement found in IgD myeloma is related to the high incidence of Bence-Jones proteinuria observed in this disease. Presenting atypical symptoms, among which renal failure is the most important, are misleading and characteristic of the disease. Survival time seems to be negatively influenced by the presence of renal failure at the time of diagnosis.

Adult↗
PubMed1988

Wolfram's syndrome and HLA.

A Sicilian family with three siblings affected by Wolfram's syndrome (Ws) is reported. HLA typing was performed in eight individuals from this family through three generations. Two of the three patients were HLA DR2 positive. The results suggest that the gene for Ws is not linked to the HLA region on chromosome 6, but located on some other chromosome, and that the allele HLA DR2 might predispose to the mutation responsible for Ws.

Adolescent↗
PubMed1987

Role of the fourth complement component (C4) in the regulation of contact sensitivity. I. Analysis in mice with high and low C4 levels.

Lymph node cells collected from CBA/J mice 4 days after painting the skin with picryl chloride are able to immunize naive recipients by hapten-IgM immuno complexes. These cells ("4-day" cells) activate the early components of the classical pathway of complement from mice of the H-2 Sd haplotype (high-C4), but fail to activate the classical pathway of complement from mice of the H-2 Sk haplotype (low-C4). Incubation of "4-day" cells in complement from mice with high-C4 levels abolishes the induction of contact sensitivity, probably as a consequence of the solubilization of membrane-bound immuno complexes caused by complement activation. The presence of "4-day" cells is determined by the levels of C4. In fact, using strains of mice which differ only at the S region of the H-2 complex, we found that mice of the H-2 Sd (and perhaps H-2 Sb) haplotype (high-C4 levels) lack "4-day" cells in their lymph nodes and this is due to the activation of the early components of the classical complement pathway which occurs in vivo in these mice during sensitization with picryl chloride. The finding that contact sensitivity reaction to picryl chloride in H-2 Sk mice lasts about 21 days, whereas H-2 Sd mice show a contact sensitivity reaction until 7 days after sensitization, strongly suggests that the S region, and in particular C4 levels, controls the persistence of "4-day" immunogenic cells, and so play a role in the duration of the contact sensitivity reaction to picryl chloride in the mouse.

Animals↗
PubMed1987

Lamin B autoantibodies in sera of certain patients with systemic lupus erythematosus.

Sera from four patients with systemic lupus erythematosus containing antibodies that yield nuclear rim staining of HEp-2 cells by indirect immunofluorescence were identified and characterized. Each serum contained autoantibodies reacting strongly with lamin B on western blots. One of the four sera displayed weaker reactivity with lamins A and C, while the other three displayed only minimal reactivity with lamins A and C. Titers of antilamin antibodies ranged from 1:1,250 to 1:36,250. Two of the sera also reacted at a dilution of 1:20 with cytoplasmic filaments of PTK-2 cells, suggesting that a small fraction of the autoantibodies in these sera may bind to alpha-helical domains of the lamins that are homologous to those of intermediate filaments. The majority of the antilamin antibodies in these patients' sera are specific for portions of the lamin B molecule that are not homologous to lamins A and C, however. The findings suggest that autoantibodies to the nuclear lamina may, in some instances, be responsible for a rim pattern in the fluorescent antinuclear antibody assay. In addition, autoantibodies to the nuclear lamina in sera of certain patients with systemic lupus erythematosus may be useful for defining the molecular structure and biological functions of lamin B, as well as for studying mechanisms of autoimmunity.

Antibody Specificity↗
PubMed1987

Effects of dextran sulphate on lymphoblast extravasation into inflammatory skin sites.

The effects of high molecular weight dextran sulphate (DXS) on the migration of 125I-labelled deoxyuridine-labelled peripheral lymphoblasts (stimulated by oxazolone) were studied in vivo by injecting the drug (50 mg/kg) subcutaneously in recipients, and by following the fate of oxazolone-stimulated peripheral lymphocytes treated in vitro with DXS in non-treated syngeneic recipients. Both types of experiments demonstrate that DXS considerably reduces lymphoblast extravasation in skin sites inflamed either by non-immune causes or by DTH. Our results also demonstrate that oxazolone-stimulated peripheral lymphocytes, after in vitro treatment with DXS, are unable to transfer antigen-specific contact hypersensitivity to unsensitized recipients. The results obtained suggest that the drug acts on both T effector cells and lymphoblasts.

Animals↗
PubMed1987

Suppression of contact sensitivity by a plastic adherent T-cell, induced in mice infected with Newcastle disease virus (NDV).

Previous studies have demonstrated that lymph node cells of mice skin-sensitized 24 h before are able to transfer contact sensitivity (CS) in naive recipients. These antigen presenting cells (APC) lose the ability to induce CS when donor mice are treated with the virus of Newcastle Disease (NDV) at the time of sensitization. In this paper we demonstrate that the cell capable of suppressing CS is a virus induced plastic adherent T-cell, which inhibits otherwise normal APC. In fact, the APC in infected mice are fully competent, as demonstrated by their ability to transfer CS, if the adherent T-cell population is removed by plastic adherence. Analysis shows that the CS suppressing adherent T-cells are Thy 1.2+, Lyt 1.1+ and I-J+ subset. The inhibition of CS by the NDV induced adherent T-cell is antigen non-specific and genetically restricted. We have also demonstrated that picrylated cells from NDV infected mice fail to trigger the release of non-specific inhibitor (nsINH) in the T-suppressor circuit. The effect of the adherent suppressor T-cell in that circuit was determined and the results indicate that the virus induced T-cell is able to suppress the release of nsINH by blocking the function of the APC.

Animals↗
PubMed1986

T suppressor afferent cells which regulate contact sensitivity to picryl chloride act across genetic barrier.

This paper investigates the requirement for genetic restriction in the action of T suppressor afferent cells (Ts-aff) which regulate the induction phase of contact sensitivity to picryl chloride. The results here reported show that Ts-aff which inhibit both the induction of contact sensitivity and DNA synthesis in the draining lymph nodes of sensitized mice, act across both H-2 and Igh genetic barrier and constitute new evidence which discriminates between two T suppressor cell populations in contact sensitivity.

Animals↗
PubMed1986

Inhibition of lymphocyte mitogenesis in mice infected with Newcastle disease virus: viral interference with the interleukin system.

Spleen cells from mice infected with Newcastle disease virus (NDV) fail to proliferate when cultured with allogeneic cells or with concanavalin A (Con A). This failure is not due to impairment of interleukin-1 (IL-1) production or to a lack of accessory cell function as stimulator cells from NDV-infected mice induce DNA synthesis in the mixed lymphocyte reaction. However, spleen cells from NDV-infected mice fail to produce detectable amounts of interleukin-2 (IL-2) when stimulated with mitogenic doses of Con A and do not respond to exogenous IL-2-containing preparations. Furthermore, absorption experiments suggest that cells from NDV-infected mice fail to bind appreciable amounts of exogenous IL-2. All these events seem to be infection-dependent, as cells from mice injected with ultraviolet-inactivated NDV (UV-NDV) behave normally.

Animals↗