Background: Altered basophil identification markers have been discovered to associate with allergic asthma (AA) in recent years. However, little is known about the expression of basophil markers in blood granulocytes.Aim: To parallel test blood basophils in peripheral blood mononuclear cell (PBMC) and granulocyte populations of patients with AA and AA combined with allergic rhinitis (ARA)Methods: The expressions of surface molecules were determined via flow cytometry. CD123 expressing cells in blood were isolated using a cell sorting technique, and mouse AA models were employed for in vivo study.Results: The numbers of CD123+HLA-DR− cells in the granulocytes of AA and ARA patients markedly increased. However, only 49.7% of CD123+HLA-DR− cells in granulocytes and 99.0% of CD123+HLA-DR− cells in PBMCs were basophils. Almost all CD123+HLA-DR− cells expressed CD63 regardless in granulocytes or PBMC. The numbers of CD63, Fc epsilon receptor I (FcεRI), and CD203c expressing cells markedly enhanced in CD123+HLA-DR− granulocytes of AA and ARA patients. Mean fluorescence intensity (MFI) of CD63 and CD203c expressions on CD123+HLA-DR− PBMC and granulocytes of AA and ARA patients dramatically elevated. House dust mite extract (HDME) and Artemisia sieversiana wild allergen extract (ASWE) enhanced the numbers of CD63+CD123+HLA-DR− granulocytes and PBMC and the MFI of CD203c expression on CD123+HLA-DR− granulocyte of AA and ARA patients. Histamine, tryptase, and PGD2 enhanced proportions of CD123+ KU812 cells. ASWE- and HDME-induced AA mice showed upregulated CD63 expression on basophils. In conclusion, upregulated expressions of CD123, CD203c, CD63, and FcεRIα in PBMC and granulocytes of patients with AA and ARA suggest that CD123+HLA-DR− cells may contribute to the development of AA and ARA.

Interleukin (IL)‐18 is a potentially important molecule in allergic rhinitis (AR). However, expressions of IL‐18, IL‐18 binding protein isoform a (IL‐18BPa) and IL‐18 receptor alpha (IL‐18Rα) in AR blood monocytes remain obscure. We, therefore, investigated IL‐18, IL‐18BPa and IL‐18Rα expressions in monocytes using flow cytometry, murine AR model and quantitative real‐time polymerase chain reaction (PCR). The results showed that the numbers of IL‐18+ monocytes increased, whereas IL‐18BPa+ monocytes decreased in the peripheral blood of AR patients. It was also observed that Platanus pollen extract provoked elevated expressions of IL‐18 and IL‐18Rα in the monocytes of AR patients. House dust mite extract, Artemisia sieversiana wild extract and Platanus pollen extract enhanced IL‐18Rα protein and mRNA expression in the isolated primary monocytes from AR patients. Using ELISA kits, we observed that the levels of total IL‐18 and free IL‐18 in the plasma of perennial AR (pAR) and seasonal AR (sAR) patients were elevated, and the molar concentration ratio of free IL‐18BPa/free IL‐18 was 16.5 for healthy control subjects and 9.7 for patients with sAR, indicating that IL‐18 likely plays a role in sAR. In the murine AR model, the number of IL‐18Rα+ monocytes increased in the blood, and the number of IL‐18Rα+ macrophages increased in the nasal lavage fluid of WT mice. In conclusion, IL‐18 may serve as a causative factor for AR.

Background: Interleukin (IL)-18 is emerging as an attractive participant in allergic rhinitis (AR). However, correlation of IL-18 with IL-18 binding protein (BP) in plasma, and expression of IL-18, IL-18BP and IL-18 receptor (R) in AR blood monocytes remain obscure.Methods: We investigated IL-18, IL-18BP and IL-18R expression in monocytes by using flow cytometric analysis, murine AR model, and quantitative real-time PCR in the present study.Results: It was found that plasma IL-18 and IL-1β in AR patients was higher than those in healthy control subjects. Free (f)IL-18 had a high correlation with IL-18BP, IL-1β and TNF-α in AR plasma. Proportion of IL-18 + monocytes was increased, whereas IL-18BP + monocytes were decreased in blood of patients with AR. It was found that Platanus pollen allergen extract provoked the elevated expression of IL-18 and IL-18R in AR blood monocytes. Dermatophagoides pteronyssinus , Artemisia sieversiana wild and Platanus pollen allergen extracts enhanced IL-18R protein and mRNA expression in primary monocytes from AR patients. Moreover, numbers of macrophages and IL-18R + macrophages in nasal lavage fluid (NLF) were increased, and levels of IL-18 in both plasma and NLF were elevated in AR mice.Conclusions: IL-18 is likely to participate in the development of AR as a causative factor, therefore, it could be a therapeutic target for AR.