Restoration by levamisole of endotoxin-inhibited neutrophil migration, oedema and increased vascular permeability induced by carrageenin.

Intravenous administration of E. coli lipopolysaccharide (LPS) inhibited the migration of neutrophils into the pleural cavity that occurs following challenge with intrapleural carrageenin. Treatment of animals with levamisole (10 mg/kg i.p.) 30 min after the intravenous administration of LPS almost restored carrageenin-induced neutrophil migration to control levels without affecting the number of circulating neutrophils. Intravenous administration of LPS (30 micrograms/kg) blocked neutrophil migration in vivo and significantly reduced the oedema and the increased vascular permeability induced by intraplantar administration of carrageenin. These LPS effects were partly counteracted by levamisole (10 mg/kg) given 30 min after LPS. Intravenous LPS did neither affect oedema nor the increase in vascular permeability induced by intraplantar administration of dextran. It is suggested that (a) the exudation and oedema formation induced by carrageenin partially depend upon migrating neutrophils and (b) inhibition of cell migration by circulating LPS may constitute an important contributing factor in septicaemia. Levamisole restores both cell migration and vascular inflammatory events inhibited by circulating LPS.