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Biomedical subjects

D Gemsa

Publications and source records attributed to D Gemsa.

At least 145 records · Page 8Linked to original sources
PubMed1979

Depressed prostaglandin release from peritoneal cells induced by a T cell adjuvant, lentinan.

PGE and PGF release from peritoneal exudate cells was studied in mice after injection with two beta (1-3) glucans, the antitumor active lentinan and the inactive pachyman, 4 days after injection of both polysaccharides, the spontaneous and phagocytosis-induced PGE and PGF release was markedly suppressed. However, only the immunopotentiator lentinan induced peritoneal exudate cells which exhibited a longer lasting diminished PG release. The data suggest that the T cell adjuvant lentinan may potentiate cellular immune responses by reducing synthesis of immune suppressive prostaglandins from peritoneal exudate cells.

Adjuvants, Immunologic↗
PubMed1978

Contribution of immunoglobulins M and G, complement, and properdin to the intracellular killing of Escherichia coli by polymorphonuclear leukocytes.

The effect of immunoglobulins and complement (C) on phagocytosis and intracellular killing of Escherichia coli was studied in vitro. The incubation system consisted of monolayers of human polymorphonuclear leukocytes and C-resistant, [3H]thymidine-labeled E. coli C source was human serum deprived of immunoglobulins and properdin by immunoabsorption. In the absence of C, only immunoglobulin G-coated bacteria were phagocytosed, whereas immunoglobulin M lacked opsonic activity. In the presence of C, phagocytosis was enhanced; however, immunoglobulin M was now more efficient than immunoglobulin G. Intracellular killing was notably augmented when C was activated by immunoglobulin G- or immunoglobulin M-coated bacteria; in contrast, the alternative activation of C by properdin had no effect on phagocytosis or intracellular killing. These results demonstrate the importance of immunoglobulins together with C not only for phagocytosis but also for efficient intracellular killing.

Cells, Cultured↗
PubMed1978

Activation of complement by radiographic contrast media: generation of chemotactic and anaphylatoxin activities.

Iodinated radiographic contrast media such as methylglucamine diatrizoate and sodium ioglycamate activate serum complement in vitro. This was shown by a dose-, time-, and temperature-dependent decrease of total hemolytic complement activity in normal human serum, consumption of C4 and C6 activity, conversion of C3 to C3b, and generation of C5-derived chemotactic and smooth muscle contracting activity. Complement activation was achieved even in sera depleted of immunoglobulin and properdin, which may indicate that contrast media induce complement activation by mechanisms different from the classical or alternative pathway.

Anaphylatoxins↗
PubMed1978

Chemotactic activity of lectins in vitro.

The effects of concanavalin A (Con A) and leucoagglutinin (LA) on the locomotor response of phagocytes have been studied in vitro. At concentrations of 1 to 4 microgram/mol, Con A and LA induced maximal chemokinesis and chemotaxis of monocytes, macrophages and, to a lesser degree, also of neutrophils. The lectin-induced locomotion was accompanied by membrane alterations and metabolic changes, as shown by an increase of the 3H-uridine uptake and a rise of the hexose monophosphate shunt activity. The chemotactic activity of Con A was inhibited by alpha-methyl mannoside (50 mM) or by pretreatment of the cells with trypsin. These data indicate that lectins such as Con A induce chemotaxis by a specific binding to receptors of the cell membrane. It is suggested that bivalent ligand binding is required as a signal to elicit chemotactic locomotion.

Agglutinins↗
PubMed1977

Enhancement of the PGE1 response of macrophages by concanavalin A and colchicine.

The effect of concanavalin A (Con A) and colchicine on the prostaglandin E1 (PGE1)-mediated cyclic AMP generation in rat peritoneal macrophages have been studied. Although Con A and colchicine by themselves did not affect cyclic AMP levels, they greatly enhanced cyclic AMP production induced by PGE1. There was not only augmentation of cyclic AMP levels at maximally active concentrations of PGE1, but also an increased sensitivity to low (inactive) concentrations of PGE1. Except for lentil lectin, none of the other lectins affected PGE1 sensitivity whereas lumicolchicine was as effective as colchicine. In addition, both Con A and colchicine raised the sensitivity to isoproterenol and choleraenterotoxin. Although details of the mechanisms by which Con A or colchicine influenced the membrane-bound adenyl cyclase and PGE1 receptors remain unclear, these observations suggest that certain alterations of the cell membrane may render macrophages more susceptible to the regulating effects of prostaglandins.

Adenylyl Cyclases↗
PubMed1975

Release of cyclic AMP from macrophages by stimulation with prostaglandins.

The effect of various prostaglandins (PG)on the generation of cyclic AMP in rat peritoneal macrophages has been studied in vitro. PGE1 produced a rapid intracellular accumulation of cyclic AMP which was followed by its release into the extracellular space. More cyclic AMP was released with prostaglandins of the E-type than with A- and F-types. It is suggested that release of cyclic AMP from macrophages may participate in the modulation of leukocyte function.

Animals↗
PubMed1974

Stimulation of heme oxygenase in macrophages and liver by endotoxin.

In rat peritoneal macrophages, engaged in erythrophagocytosis in vitro, endotoxin stimulated heme oxygenase (HO) activity, which was additive to the substrate-mediated enzyme induction produced by the ingested erythrocyte hemoglobin. Endotoxin neither appeared to injure the erythrocytes, nor did it enhance the rate of erythrophagocytosis. In intact rats, HO activity in both parenchymal and sinusoidal cells of the liver was increased after treatment with endotoxin. It is likely that endotoxin directly stimulates HO activity, a process which may account for the reported rise in bilirubin formation in endotoxin-treated animals. The effect of endotoxin on HO may represent part of the general activation of phagocytic cells by endotoxin.

Animals↗