A new water-soluble, orally absorbable de-N-acetyl-lysoganglioside (WI
LD20), breakdown product of the monosialoganglioside GM(1), was found
to influence some parameters of neutrophil response to inflammation st
imuli. Superoxide anion production appears inhibited, along with neutr
ophil 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 signifi
cant reduction of neutrophils observed at the site of inflammation, wh
ichever agonist was used. The effects on neutrophil physiology found i
n normal or in pathological conditions, are in favour of a WILD20-rela
ted inhibitory effect on neutrophil contribution to inflammation.