GALACTOSE TERMINATED OLIGOSACCHARIDES ACTIVATE MACROPHAGE RESPIRATORY BURST

Respiratory burst is a primary event exhibited by macrophages in response to specific stimuli. We present results on activation of respiratory burst by lactose and sialyl lactose which were comparable to that of known activators like phorbol ester, lipopolysaccharide and Ca2+-ionophore. These oligosaccharides were used as models of erythrocyte membrane glycoproteins whose terminal sugars are either galactose or sialic acid. Maximum activation at as low as 3 pM or 6 pM of sialyl lactose or lactose was obtained while desialylated erythrocyte membranes (5 ng) with exposed beta-galactosyl residues containing small amounts of sialic acid proved to be effective activators of respiratory burst. We could establish from kinetics of activation that maximum respiratory burst occurs between 5-9 min with either oligosaccharides or membranes as activators. The probable mechanism of activation by oligosaccharides and membranes was found to be operating via protein kinase C or calmodulin signal mediation pathways and inhibition by intracellular cAMP suggests the role for dephosphorylation and inactivation of respiratory burst. Taken together, our results suggests that exposed beta-galactosyl residues are capable of triggering the generation of reactive O2 species which are implicated in killing and digestion of the engulfed organisms by phagocytes.