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R B Cogen

Publications and source records attributed to R B Cogen.

24 records · Page 2Linked to original sources

Detachment of endothelial cells by polymorphonuclear leukocytes in vitro: potentiation by antibody coating and prevention by inflammatory exudate.

A widely advocated hypothesis suggests that polymorphonuclear leukocytes release enzymes at sites of inflammation which in turn cause tissue damage, especially vasculitis. To test this we isolated and grew human endothelial cells and labelled them with chromium-51. Polymorphonuclear leukocytes were separated from whole blood and added to the labelled endothelial cells. Upon incubation with the polymorphonuclear leukocytes the endothelial cells rapidly detached but were not lysed. Detachment was prevented by the addition of small amounts of inflammatory exudate. Prior coating of endothelial cells with a specific antibody accelerated detachment of the cells by polymorphonuclear leukocytes but this was still prevented by addition of inflammatory exudate in low concentration. In a separate experiment extracellular basement membrane synthesized in vitro by endothelial cells was labelled by incubating the cells with 14C-proline. Polymorphonuclear leukocytes caused release of 14C but this was again prevented by addition of either inflammatory exudate or serum. We conclude that polymorphonuclear leukocytes alone could cause vascular intimal damage in vivo if inhibitors, which are present in serum and inflammatory exudate, are excluded or overwhelmed.

Antibodies↗

Cell-detaching activity mediated by an enzyme(s) obtained from human leukocyte granules.

Granule proteins have been isolated from human peripheral blood leukocytes and their effects on intact tissue culture cells have been determined. Three hours after the addition of the mixture of granule hydrolases, both HeLa cells and human newborn fibroblasts were detached from one another and from their growth surface, but they seemed to remain viable, since cell-bound -51Cr was retained. Further studies with HeLa cells indicated that after as long as 24 hours in the presence of these enzymes the cells remained viable as judged by several independent criteria. The enzyme activity responsible for cell detachment was subject to inhibition by various protease inhibitors. Its molecular size, as determined by gel filtration, was approximately 20,000 daltons. In addition, the naturally occurring serum inhibitor of this enzyme activity was characterized as either alpha(1)-antitrypsin or another protein with similar properties.

Cell Adhesion↗

Immunoglobulin molecules on the surface of activated T lymphocytes in the rat.

Lewis strain rat lymphocytes were exposed in vitro to a variety of specific and nonspecific blastogenic stimuli. The surfaces of the transformed lymphocytes were examined by indirect immunofluorescence for the presence of T cell antigens and immunoglobulin molecules. More than 90% of lymphocytes that underwent blast transformation after exposure to foreign histocompatibility antigens (mixed lymphocyte reaction; in vitro allograft reaction), purified tuberculin, phytohemagglutinin (PHA), and concanavalin A (Con-A) had T cell antigenic markers on their surfaces. 70-92% of the antigen-stimulated blast cells also had readily detectable surface immunoglobulin molecules, whereas less than 3% of the PHA- and Con-A-activated cells were Ig(+). Pokeweed mitogen (PWM) appeared to activate both B and T cells, but the T cells did not have detectable surface immunoglobulin molecules. Nonactivated control cultures contained T(+)Ig(-) lymphocytes almost exclusively. The results suggest that thymus-dependent rat lymphocytes express increased amounts of detectable immunoglobulin on their surface in response to specific stimulation with antigen. It is postulated that the acquisition of immunological competence by activated T cells may be related to this expression of surface immunoglobulin.

Animals↗