Polymorphonuclear leucocytes (PMNL) undergo a marked activation of their oxidative metabolism upon interaction with surface-reactive soluble stimuli as well as with phagocytosable objects. To get some insight into the mechanism of this stimulation, we have compared the stimulatory activity of the tetravalent lectin concanavalin A (Con A) with that of the divalent derivative succinyl-Con A (S-Con A). Both lectins bind to the PMNL surface to the same extent. S-Con A, however, is much less efficient in stimulating the PMNL metabolism. When S-Con A-treated PMNL are further reacted with antiserum to Con A, a potentiation of the metabolic stimulation is observed. Normal serum or addition to PMNL of antiserum to Con A in the absence of lectin has no effect. Furthermore, if S-Con A is displaced from its receptors on the cell membrane with alpha-methyl mannopyranoside, the addition of antiserum fails to cause a respiratory stimulation. These results suggest that the initial triggering of the metabolic stimulation of PMNL is in part accomplished through cross-linkage of membrane constituents.
Metabolic stimulation of polymorphonuclear leucocytes: effects of tetravalent and divalent concanavalin A
BERTON, Giorgio;
1978-01-01
Abstract
Polymorphonuclear leucocytes (PMNL) undergo a marked activation of their oxidative metabolism upon interaction with surface-reactive soluble stimuli as well as with phagocytosable objects. To get some insight into the mechanism of this stimulation, we have compared the stimulatory activity of the tetravalent lectin concanavalin A (Con A) with that of the divalent derivative succinyl-Con A (S-Con A). Both lectins bind to the PMNL surface to the same extent. S-Con A, however, is much less efficient in stimulating the PMNL metabolism. When S-Con A-treated PMNL are further reacted with antiserum to Con A, a potentiation of the metabolic stimulation is observed. Normal serum or addition to PMNL of antiserum to Con A in the absence of lectin has no effect. Furthermore, if S-Con A is displaced from its receptors on the cell membrane with alpha-methyl mannopyranoside, the addition of antiserum fails to cause a respiratory stimulation. These results suggest that the initial triggering of the metabolic stimulation of PMNL is in part accomplished through cross-linkage of membrane constituents.
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