Efficient Induction of Superoxide Release from Human Neutrophils by the Galactoside-Specific Lectin fromViscum album

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Abstract
The immunomodulatory galactoside-specific lectin from Viscum album (VAA) induces superoxide anion (O2.-) release from human neutrophils. Among twelve tested lectins, VAA, has the highest activity, clearly surpassing the effect of the human beta-galactoside-specific lectin (galaptin). Its reactivity is blocked in the presence of lactose and is strictly dependent on the carbohydrate-binding B-subunit. The toxic A-subunit of the lectin does not elicit a response. The VAA-induced respiratory burst is less sensitive to addition of adenosine and theophylline than the concanavalin A-mediated reaction. Other modulators like amiloride (up to 100 microM), trifluoperazine and N-ethylmaleimide reveal less pronounced differences, and indomethacin, colchicine (up to 100 microM) as well as cytochalasin B act as stimulators of lectin-induced O2.- release from neutrophils. The O2.- production in the presence of small concentrations of VAA (0.1-20 micrograms/ml) is increased by addition of N-formylmethionyl-leucyl-phenylalanine (FMLP), phorbol 12-myristate 13-acetate (PMA) or digitonin, respectively, whereas concanavalin A (Con A) or wheat germ agglutinin (WGA) fail to affect the VAA-dependent extent of the respiratory burst. These results substantiate that the VAA-induced O2.- release from human neutrophils can be enhanced by other classes of inductors.