Sugar-Specific Inhibitory Effects of Wheat Germ Agglutinin and Phytohemagglutinin-E4 on Histamine Release Induced by Basic Secretagogues from Rat Peritoneal Mast Cells and Their Possible Action Sites

Abstract

ABSTRACT-The histamine release induced by compound 48/80, bradykinin or polyethylenimine with a molecular weight of 600 (PEI6) was inhibited by wheat germ agglutinin (WGA) and phytohemagglutinin E-subunits (PHA-E4), and the inhibition was specifically reversed by N-acetyl glucosamine and N-acetyl galactosamine, respec tively. Concanavalin A (Con A) and phytohemagglutinin L-subunits (PHA-L4) did not inhibit the histamine release induced by compound 48/80, bradykinin or PEI6. The histamine release induced by substance P was also inhibited sugar-specifically by WGA and PHA-E4. The binding sites for compound 48/80, bradykinin, PEI6 and sub stance P, therefore, seemed to especially overlap each other. These binding sites were found to be glycoproteins having affinities to WGA and PHA-E4, but not to Con A and PHA-L4. The binding of WGA and PHA-E4 to the glycoproteins resulted in inhibition of the interaction between the basic secretagogues including bradykinin and substance P and their binding sites on the mast cells. The bindings of five lectins to mast cell glycoproteins were examined by lectin-blotting. Several glycoproteins, which had specific affinities to WGA and PHA-E4, but not to Con A and PHA-L4 were de tected. We assumed that the binding sites for basic secretagogues which are coupled with histamine-releasing mechanisms exist among these glycoproteins. A 41-kDa pro tein (a-subunit of pertussis toxin-sensitive G protein) was not detected by WGA, sug gesting that the binding sites for the basic secretagogues were not G proteins.Stimulus-secretion coupling mechanisms in rat peritoneal mast cells are thought to involve G proteins, because GTP-analogues enhanced histamine release (1). Moreover, histamine re lease induced by compound 48/80 or brady kinin is inhibited by pertussis toxin, but that induced by antigen or anti-IgE is not (2-4). We found that the histamine release induced by polyethylenimine (MW = 600, PEI6) was inhibited by pertussis toxin (5). Compound 48/80, bradykinin and polyethylenimine are all basic secretagogues. There is, however, no similarity in their chemical structures. The ac tion sites for compound 48/80 on the plasma

Datura stramonium Agglutinin Released Histamine from Rat Peritoneal Mast Cells That Was Inhibited by Pertussis Toxin, Haptenic Sugar and N-Acetylglucosamine-Specific Lectins: Involvement of Glycoproteins with A-Acetylglucosamine Residues

“…In this study, we proposed that the binding of DSA to the corresponding glyco proteins resulted in histamine release and that WGA, STA and PWM inhibited it. These results were consistent with the inhibitory effects of lectins on the histamine release in duced by basic secretagogues (9,10). The binding of Con A to the glycoproteins including the IgE-IgE receptor complex, however, did not inhibit the histamine release induced by DSA, and a-MM, a haptenic sugar of Con A, was not inhibitory.…”

“…They lack responsiveness to non-immunologic stimuli, although they begin to respond to compound 48/80 after co-cul ture with fibroblasts (8). Recently we reported that a 10 min incubation of specific lectins with rat peritoneal mast cells resulted in the inhibition of the histamine release in duced by compound 48/80, bradykinin and PEI6 (9,10). The inhibitory lectins for the histamine release induced by compound 48/80, bradykinin or PEI6 were WGA (9), PHA-E4 (9) and STA (10), as well as MAM (10).…”

Inhibitory Effects of Sialic Acid- or N-Acetylglucosamine-Specific Lectins on Histamine Release Induced by Compound 48/80, Bradykinin and a Polyethylenimine in Rat Peritoneal Mast Cells

“…Glycoproteins were detected by WGA and PHA-E4-blotting, but glycolipids were not (17). Because WGA and PHA-E4 are G1cNAc specific, especially the bisecting GIcNAc-specific lectins, glycoproteins with G1cNAc-residues seemed to be in volved in the histamine releasing mechanisms, and the binding of WGA and PHA-E4 to the glycoproteins result ed in inhibition of histamine release.…”

“…Recently our group reported that a 10-min incubation of rat peritoneal mast cells with WGA or PHA-E4, but not with Con A or PHA-L4, resulted in sugar-specific inhi bition of the histamine release induced by compound 48/80, bradykinin and PEI6 (14,17). Glycoproteins were detected by WGA and PHA-E4-blotting, but glycolipids were not (17).…”

D-Galactose-Specific Sea Urchin Lectin Sugar-Specifically Inhibited Histamine Release Induced by Datura stramonium Agglutinin: Differences Between Sugar-Specific Effects of Sea Urchin Lectin and Those of D-Galactose- or L-Fucose-Specific Plant Lectins

“…Among the activators of the IgE-independent pathway, DSA is a lectin having affinity to GlcNAc oligomers. Moreover, our group observed that lectins with affinity to GlcNAc and /or sialic acid (Sia) inhibited histamine release induced by compound 48 / 80, substance P and DSA (5,11,12). On the other hand, the effects of D(+)Gal-, N-acetyl galactosamine (GalNAc)-and L(-)Fuc-specific lectins on the activation of mast cells induced by compound 48/80, substance P and DSA are unknown.…”