Background: Recently we have shown that anti-acid drugs lead to an enhanced risk of food allergy. This may be due to hindered peptic digestion, caused by an elevation of the gastric pH. Additionally, it is known that aluminium-linked antigens lead to an increased probability of sensitization.
Objective: Our aim in this study was to show whether sucralfate promotes sensitization not only by preventing peptic digestion but also by acting as a T-helper type 2 (Th2) adjuvant.
Methods: To avoid the effect of sucralfate on the gastric pH and to show only the adjuvant effect, BALB/c mice were immunized on the parenteral route with codfish extract plus sucralfate, and control groups with aluminium hydroxide (alum) (Th2 adjuvant) or monophosphoryl lipid A (MPL) (Th1 adjuvant). Antigen-specific antibodies and cytokine levels were determined. The in vivo effect was investigated by intradermal skin tests.
Results: Codfish-specific high IgG1 and IgE antibody levels as well as elevated IL-4 and IL-5 levels in alum- and MPL-treated mice, but more importantly also in sucralfate-treated mice, indicated a Th2 shift. Positive skin tests confirmed this Th2 response.
Conclusions: Our data show that parenterally applied sucralfate is able to induce a Th2 response probably due to the aluminium content. This indicates that orally applied sucralfate may lead to an enhanced risk of food allergy not only by inhibiting peptic digestion but also by acting as a Th2 adjuvant.
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