A major factor in non-allergic
food hypersensitivity could be the interaction of dietary
lectins with mast cells and basophils. Because
immunoglobulin E (
IgE) contains 10-12%
carbohydrates,
lectins can activate and degranulate these cells by cross-linking the
glycans of cell-bound
IgE. The present objective focuses on the effect of
potato lectin (
Solanum tuberosum agglutinin; STA) for its ability to release
histamine from basophils in vitro and mast cells in vivo from non-atopic and atopic subjects. In this study, subjects were selected randomly based on case history and skin prick test responses with food, pollen and house dust mite extracts. Skin prick test (SPT) was performed with STA at 100 microg/ml concentration. Histamine release was performed using leucocytes from non-atopic and atopic subjects and rat peritoneal exudate cells. SPT on 110 atopic subjects using STA showed 39 subjects positive (35%); however, none showed STA-specific
IgE; among 20 non-atopic subjects, none were positive by SPT. Maximal histamine release was found to be 65% in atopic subjects (n = 7) compared to 28% in non-atopic subjects (n = 5); the release was inhibited specifically by oligomers of
N-acetylglucosamine and correlates well with serum total
IgE levels (R(2) = 0.923). Binding of STA to N-linked
glycoproteins (
horseradish peroxidase,
avidin and
IgG) was positive by dot blot and binding assay. As
potato lectin activates and degranulates both mast cells and basophils by interacting with the
chitobiose core of
IgE glycans, higher intake of potato may increase the clinical symptoms as a result of non-allergic
food hypersensitivity in atopic subjects.