wild-20 and Inflammation

wild-20 has been researched along with Inflammation* in 1 studies

Other Studies

1 other study(ies) available for wild-20 and Inflammation

Article	Year
In vitro and in vivo impact of a new glycosphingolipid on neutrophils. Agents and actions, 1994, Volume: 42, Issue:3-4 A new water-soluble, orally absorbable de-N-acetyl-lysoganglioside (WILD20), breakdown product of the monosialoganglioside GM1, was found to influence some parameters of neutrophil response to inflammation stimuli. Superoxide anion production appears inhibited, along with neutrophil killing properties. A block of both pathways of arachidonic acid cascade and PAF was also found, as well as neutrophil ICAM-1-mediated adhesion to endothelial cells. Of particular interest was the significant reduction of neutrophils observed at the site of inflammation, whichever agonist was used. The effects on neutrophil physiology found in normal or in pathological conditions, are in favour of a WILD20-related inhibitory effect on neutrophil contribution to inflammation. Topics: Animals; Bone Marrow; Bone Marrow Cells; Calcimycin; Cell Adhesion; Chemotaxis, Leukocyte; Eicosanoids; Erythrocytes; Gangliosides; Hemolysis; Humans; In Vitro Techniques; Inflammation; Leukocyte Count; Mice; Neutrophils; Phagocytosis; Platelet Activating Factor; Platelet Aggregation Inhibitors; Superoxides	1994

Article

Year

In vitro and in vivo impact of a new glycosphingolipid on neutrophils.

Agents and actions, 1994, Volume: 42, Issue:3-4

A new water-soluble, orally absorbable de-N-acetyl-lysoganglioside (WILD20), breakdown product of the monosialoganglioside GM1, was found to influence some parameters of neutrophil response to inflammation stimuli. Superoxide anion production appears inhibited, along with neutrophil killing properties. A block of both pathways of arachidonic acid cascade and PAF was also found, as well as neutrophil ICAM-1-mediated adhesion to endothelial cells. Of particular interest was the significant reduction of neutrophils observed at the site of inflammation, whichever agonist was used. The effects on neutrophil physiology found in normal or in pathological conditions, are in favour of a WILD20-related inhibitory effect on neutrophil contribution to inflammation.

Topics: Animals; Bone Marrow; Bone Marrow Cells; Calcimycin; Cell Adhesion; Chemotaxis, Leukocyte; Eicosanoids; Erythrocytes; Gangliosides; Hemolysis; Humans; In Vitro Techniques; Inflammation; Leukocyte Count; Mice; Neutrophils; Phagocytosis; Platelet Activating Factor; Platelet Aggregation Inhibitors; Superoxides

1994