Zinc treatment prevents IgE-mediated Ca 2+ influx and allergic response in RBL-2H3 cells.

Zinc (Zn) is an essential metal in the body. It binds to many proteins and regulates their functions. In the immune system, it is known that administration of ZnSO ₄ suppresses T cell activation, but its effects on allergies are still unknown. In this study, we investigated the effects of ZnSO ₄ administration on allergic reactions using the rat basophilic leukemia cell line, RBL-2H3. ZnSO ₄ treatment inhibited cell degranulation induced by antigen and IgE stimulation, as well as by A23187, a Ca ²⁺ ionophore. Antigen and IgE stimulation increased mRNA expression of IL-4, IL-13, and COX-2, and ZnSO ₄ treatment inhibited this expression. The elevation of intracellular Zn concentration and depletion of Zn did not affect degranulation. Phosphorylation of the proteins spleen tyrosine kinase, p38, ERK1/2, JNK, and Akt was increased by antigen stimulation, but ZnSO ₄ treatment did not inhibit this phosphorylation. ZnSO ₄ treatment inhibited the elevation of intracellular Ca ²⁺ concentration induced by antigen and IgE stimulation, as well as by A23187. Additionally, ZnSO ₄ treatment inhibited thapsigargin, a store-operated Ca ²⁺ entry stimulant, from inducing degranulation and increasing intracellular Ca ²⁺ concentration. These data indicate that exogenous Zn ²⁺ possesses a preventive effect on RBL-2H3 activation via inhibition of Ca ²⁺ influx. The effect of Zn may involve Ca ²⁺ release-activated channels. This study suggests that ZnSO ₄ treatment is valuable in suppressing allergic responses.
Competing Interests: Declaration of competing interest We declare that there are no conflicts of interest to disclose.
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