Regulatory Role of Zinc in Allergic Rhinitis through the IL-33/ST2 Pathway

OBJECTIVE: We aimed to investigate the expression of serum zinc and cytokines interleukin- (IL-) 13 and IL-33 in patients with allergic rhinitis (AR) and observe the effects of zinc on cytokines and pathway proteins in P815 mast cells stimulated by Artemisia annua allergen (Art.) in the IL-33/suppression of the tumorigenicity 2 (ST2) pathway. We also aimed to explore the possible regulatory role of zinc in AR and provide new ideas to determine the etiology and treatment of AR. METHODS: AR patients treated from March to September in 2018 were selected as the research participants, and 50 healthy people in the same period were selected as the control group. Serum samples of all patients were collected, and those of AR patients were tested for the presence of allergens. The expression of IL-13 and IL-33 was detected by performing an enzyme-linked immunosorbent assay, while the serum zinc level was detected by conducting an inductively coupled plasma mass spectrometry. The cell counting kit (CCK-8) was used to detect the proliferation of P815 mast cells, and western blot was used to detect the expression of ST2, p38, and p65 proteins. RESULTS: A total of 92 AR patients were included in the study; of them, 52 had mild AR, while 40 had moderate AR. The primary allergen found in AR patients was Artemisia, and the positivity rate was 53.26%. The serum zinc ion level of AR patients decreased, and the expression of IL-13 and IL-33 increased. After Art. was used to treat P815 mast cells, the expression of IL-33 in the cell supernatant increased in a concentration-dependent manner, the expression of receptor ST2 increased, and the expression of downstream p38 and p65 proteins increased. However, after treatment with ZnSO(4), the expression of IL-33 in the cell supernatant decreased, and the expression of ST2, p38, and p65 protein decreased. CONCLUSION: The serum zinc level of AR patients decreased. In the IL-33/ST2 pathway, ZnSO(4) can reduce the hypersensitivity of mast cells induced by Art.