Tamiko Suzuki-Nishimura1,*, Hideyuki Nakagawa2 and Masaatsu K. Uchida1
1Department of Pharmacology, Meiji Pharmaceutical University, Tokyo 204-8588, Japan
2Department of Life Sciences, University of Tokushima, Tokushima 770-8502, Japan
*Corresponding author. Present address for correspondence: Pharmaceuticals and Medical Devices Evaluation Center (PMDEC), National Institute of Health Sciences (NIHS), Toranomon-33-Mori Building, Toranomon 3-8-21, Minato-ku, Tokyo 105-8409, Japan. FAX: +81-3-5403-1417
Abstract: A new sea urchin lectin from Toxopneustes pileolus, is D(+)galactose (Gal)-, D(+)fucose (Fuc)-specific. Incubation of rat peritoneal mast cells with the lectin in the presence of 0.3 mM CaCl2 for 10 min significantly and dose-dependently inhibited the histamine release induced by N-acetyl glucosamine (GlcNAc)-specific Datura stramonium agglutinin (DSA), an activator of the Gi-protein-dependent pathway in mast cells. This inhibition by the sea urchin lectin was sugar-specifically reversed in the presence of D(+)Gal or D(+)Fuc but not L(−)Fuc. The sea urchin lectin had no effect on the histamine release induced by compound 48/80, slightly inhibited the histamine release induced by substance P and mastoparan, and slightly enhanced the histamine release induced by melittin, but these effects were not dose-dependent. Compound 48/80, substance P, mastoparan and melittin are mast cell activators without sugar residues. It is suggested that the lectin binds to D(+)Gal residues of DSA to interfere with mast cell activation induced by DSA, a glycoprotein with arabinose and Gal residues. The effects of plant lectins with affinity to D(+)Gal, N-acetyl galactosamine and/or sialic acid and L(−)Fuc on the histamine release induced by DSA, compound 48/80 and substance P were also examined.
Keywords: Mast cell, Histamine release, Datura stramonium agglutinin, D(+)Galactose-specific lectin, Compound 48/80, Substance P
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