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Biomedical subjects

C Chizzolini

Publications and source records attributed to C Chizzolini.

48 records · Page 3Linked to original sources
PubMed1984

Antimalarial immunity in Saimiri monkeys. Immunization with surface components of asexual blood stages.

Plasmodium falciparum polypeptides of 200 and 140 K mol wt exposed at the surface of merozoites and/or schizonts were purified by affinity chromatography and by electroelution from sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Monkeys were separated into three groups of four and immunized either with one of the two polypeptides or with saline (control). After intravenous challenge with 2.5 X 10(7) P. falciparum asexual blood stages, two monkeys of the control group had to be treated and two recovered spontaneously after peak parasitemia of 9 and 11%. The four monkeys immunized with the 140 K polypeptide recovered without treatment after peak parasitemia between 1.5 and 4.5%. Monkeys immunized with the 200 K polypeptide had similar peak parasitemia except one monkey who suffered from a large skin excoriation and who recovered spontaneously after a peak parasitemia of 11%. Prechallenge sera of the immunized monkeys reacted only with the polypeptide used for immunization except for one serum of the 140 K group, which precipitated an additional polypeptide of 39 K, and a polypeptide of 31 K weakly precipitated by the four sera of monkeys immunized with the 200 K polypeptide. The relatedness between the 200 and 140 K polypeptides was investigated using tryptic digestion and reverse phase chromatography. No clear analogy was found between the two polypeptides, which suggests that immunization with either of two independent surface components of P. falciparum asexual blood stages is able to induce at least a partial protective immunity in immunized hosts.

Animals↗
PubMed1984

Altered expression of B lymphocyte surface immunoglobulins in minimal change nephrotic syndrome and focal glomerulosclerosis.

In 20 patients with nephrotic syndrome (10 minimal change glomerulonephritis, MCN; 10 focal glomerulosclerosis, FGS) the peripheral blood lymphocytes showed a statistically significant increase in IgG-bearing cells (SIgG-C) in comparison with 30 patients with other histological types of primary glomerulonephritis with and without nephrotic syndrome (14 and 16, respectively). In the same MCN and FGS patients the serum IgG levels were slightly decreased. Furthermore, 5 cases of MCN in sustained remission for 1 year after steroid therapy showed normalization of the SIgG-C and the serum IgG levels. The possible significance of these phenomena in the pathogenesis of the hypo-IgG-globulinemia in MCN and FGS is discussed.

Adolescent↗
PubMed1983

Minimal change glomerulonephritis and focal glomerulosclerosis markers and 'in vitro' activity of peripheral blood mononuclear cell.

Serum concentrations of IgG, IgA and IgM and PBMC were investigated in 11 prevalently adult patients with idiopathic glomerulonephritis, five minimal change glomerulonephritis (MCGN) and six focal glomerulosclerosis (FGS) and nephrotic syndrome. Among the peripheral blood mononuclear cells (PBMC) E rosette forming cells (T-cells), surface immunoglobulin bearing cells (B-cells), and T-cells with IgG Fc receptor (T gamma) were determined. In the culture supernatants of PBMC stimulated with PWM, the concentration of secreted IgG, IgA and IgM was determined by a solid phase immunofluorescence assay. After stimulation with PWM and PHA, the 3H-TdR uptake from PBMC was evaluated. In patients only the serum values of IgG were found significantly decreased. No difference was observed between patients and healthy age and sex matched controls, in percentage and absolute number of T and B-cells, whereas an increased number of T gamma was present in patients. In these patients after stimulation with PWM the production of IgG and IgA, but not IgM, and the 3H-TdR incorporation, were significantly lower than in healthy controls. These results suggest an imbalance in the cellular co-operation or an intrinsic B-cell defect in the synthesis or secretion of Ig in MCGN and FGS.

Adolescent↗
PubMedDate not supplied

Age-related prevalence of antibody response against three different, defined Plasmodium falciparum antigens in children from the Haut-Ogooué province in Gabon.

The kinetics of the humoral response to defined Plasmodium falciparum antigens was studied in 543 children, 1 month to 15 years old, living in an area endemic for malaria. The antigens used for enzyme-linked immunosorbent assay were (i) the synthetic peptide (NANP)40 representing the immunodominant repeated region of the circumsporozoite protein, and (ii) the fusion peptide 31.1, representing the N-terminal portion of the 83 kDa polypeptide expressed at the surface of merozoites which is a processed product of the 190-200 kDa glycoprotein. In addition, glutaraldehyde-fixed infected red blood cells (RBC) were used to detect ring-infected erythrocyte surface antigen (RESA) and unfixed infected RBC to detect intra-erythrocytic asexual form (IEF) antigens by immunofluorescence. In the 1 to 2 months age group, 50%, 26% and 21% of the children had antibodies for IEF, (NANP)40 and 31.1 respectively, but none had anti-RESA antibodies. The proportions of positive subjects decreased until 3 to 6 months and then increased progressively for the 4 antigens, approaching, but not reaching, adult values by the age of 15 years. Antibodies against specific antigens were acquired concomitantly. Children born from (NANP)40-positive mothers showed enhanced anti-(NANP)40 IgG responses.

Adolescent↗
PubMedDate not supplied

Adrenalectomy abolishes phosphatidylserine inhibition of lipopolysaccharide-induced tumor necrosis factor release.

The treatment with phosphatidylserine (PS) has recently been shown to inhibit in vivo the lipopolysaccharide (LPS)-induced release of tumor necrosis factor (TNF) (Monastra and Bruni, 1992, Lymphokine Cytokine Res. 11:39). The aim of the present work was to investigate the mechanism(s) involved in the inhibition by PS. No in vitro inhibition of LPS-induced TNF release was observed when PS was used in vitro with human whole blood cells. The opposite was observed, in vitro PS enhanced TNF release. Previous work has shown that PS induces histamine release by mast cells and it is known that histamine inhibits TNF release. PS treatment of W/WV mice lacking mast cells, which are therefore unable to release histamine, resulted in inhibition of LPS-induced TNF release; thus excluding a major role of histamine in mediating PS inhibition. However, in adrenalectomized mice PS treatment failed to inhibit the LPS-induced TNF release, while the effect of PS was evident in sham-operated mice. PS treatment in adrenalectomized mice was associated with an increase in TNF serum levels when compared to untreated animals. Overall these results suggest that PS inhibition of LPS-induced TNF release is dependent on adrenal hormones, while PS, in the absence of adrenal hormones, seems to have a priming effect on the cells that produce TNF after LPS stimulus.

Adrenal Cortex Hormones↗