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Biomedical subjects

J F Borel

Publications and source records attributed to J F Borel.

At least 73 records · Page 4Linked to original sources
PubMed1978

In-vivo effects of anti-inflammatory and other drugs on granulocyte emigration in the rabbit skin collection chamber.

A method for measuring localised leukocyte mobilisation under in-vivo conditions with a plastic skin collection-chamber adapted to the rabbit ear was used for assessing the effects of anti-inflammatory and other agents on granulocyte emigration. Studies on the effect of oral drug administration to rabbits indicated that most anti-inflammatory drugs, two cystostatic agents (cyclophosphamide and colchicine), but none of the other compounds exhibiting antihistaminc, beta-adrenolytic or neuroleptic properties, significantly inhibited granulocyte mobilisation. The results after topical application of some of these agents into the chamber correlated well with those obtained after oral treatment. This technique may thus prove useful in selecting new compounds inhibiting granulocyte mobilisation in acute inflammatory reactions.

Animals↗
PubMed1978

The effects of fractions (chalones) obtained from lymphoid organs on the immune response in vivo.

Aqueous extracts of calf and pig lymphoid organs were prepared and fractionated by means of gel filtration, ion exchange chromatography, and isoelectric focusing. These fractions, which had been previously assessed on mitogen-stimulated mouse spleen lymphocytes and other cells in vitro, were tested for their in vivo activity on humoral (haemolytic PFC in mice) and on cell-mediated immunity (skin allograft survival in mice, lymph node weight assay in rats, and systemic GvH-reaction in mice). None of these several fractions elicited either biologically significant or reproducible inhibitory effects. In particular, two fractions, a high and a small molecular weight fraction which were strongly inhibitory in vitro, remained without any chalone-like activity in these in vivo assays. Our results therefore failed to support the existence of a lymphocyte chalone.

Animals↗
PubMed1977

The effects of fractions (chalones) obtained from lymphoid organs on lymphocyte proliferation in vitro.

Aqueous extracts of lymphoid organs were prepared and fractionated by means of gel filtration, ion exchange chromatography, and isoelectric focusing. A protein-containing fraction with a molecular weight of approximately 80,000--90,000 and isoelectric points of 7.6 and 5.3--6.2 was isolated and shown to inhibit reproducibly both thymidine incorporation and proliferation of concanavalin A-stimulated mouse spleen lymphocytes in vitro. This effect appeared specific since proliferation of mastocytoma P-815 and leukemia L-1210 cells remained unaffected. A small molecular weight fraction (500 to 10,000 daltons) was also found to inhibit lymphocyte proliferation in vitro but was without apparent specificity for cell type.

Animals↗
PubMed1977

Effects of the new anti-lymphocytic peptide cyclosporin A in animals.

The fungus metabolite cyclosporin A is a small cyclic peptide acting as a novel antilymphocytic agent. It is effective following either parenteral or oral administration in mice, rats and guinea-pigs. The suppressive effect after short and prolonged treatment on plaque-forming cells, the inhibition of the secondary humoral response and the reversibility of its effect on haemagglutinin formation is demonstrated. Cyclosporin A inhibits delayed hypersensitivity skin reaction to oxazolone (primary and secondary responses) in mice and to tuberculin in guinea-pigs. Its failure to suppress antibody synthesis to lipopolysaccharide antigens in nude mice suggests a selective effect on T cells. High doses of the compound affect the haemopoietic tissues very weakly as shown by the bone marrow and stem cell numbers in mice, which finding markedly contrasts with most other immunosuppressive and cytostatic drugs.

Animals↗
PubMed1976

Biological effects of cyclosporin A: a new antilymphocytic agent.

The fungus metabolite cyclosporin A is a small peptide acting as a novel antilymphocytic agent. It strongly depressed appearance of both direct and indirect plaque-forming cells and produced a clear dose-dependent inhibition of haemagglutinin formation in mice upon oral administration. Skin graft rejection in mice and graft-versus-host disease in mice and rats were considerably delayed by cycloporin A which also prevented the occurrence of paralysis in rats with experimental allergic encephalomyelitis. This compound was not only highly effective in preventing development of Freund's adjuvant arthritis, but in addition improved the symptoms in rats with established arthritis, although it is inactive in acute inflammation. This new agent contrasts with other immunosuppressives and cytostatic drugs in its weak myelotoxicity. Experimental evidence suggests that cyclosporin A, rather than being cytostatic or lympholytic, affects an early stage of mitogenic triggering of the immunocompetent lymphoid cell.

Animals↗
PubMed1976

Comparative study of in vitro and in vivo drug effects on cell-mediated cytotoxicity.

Cell-mediated cytolysis (CMC) was assayed in a system using spleen cells from mice (C57BL/6) sensitized with allogeneic tumour cells (DBA/2 mastocytoma P-815). Anti-inflammatory drugs, immunosuppressives, inhibitors of cell division and other agents were investigated for their capacity to inhibit CMC in three different ways. First, inhibition of CMC after in vitro addition of drug was observed with corticosteroids, some immunosuppressives and inhibitors of cell division. Secondly, suppression of CMC after a single drug administration to sensitized mice shortly before being killed was found with corticosteroids, several immunosuppressives and irradiation. Thirdly, prevention of development of CMC by repeated drug treatment (immunosuppressive schedule) was achieved with most immunosuppressives and cytostatic drugs. Non-steroidal anti-inflammatory drugs were inactive in these tests. Correlation of effects between the three procedures was very poor and it is suggested that various mechanisms may be involved in the different assays.

Animals↗
PubMed1975

Chemotaxis of rabbit macrophages in vitro: inhibition by drugs.

Chemotaxis of rabbit macrophages was inhibited by phenylbutazone and sodium salicylate, but not by other antiinflammatory agents. Other inhibitory compounds were colchicine, vincristine, PHA, Con A, iodoacetic acid, cytochalasin B, and EDTA. Some of these in vitro results contrast apparently with in vivo effects.

Animals↗