%0 Generic %A Y., Hiraguchi %A H., Tanida %A M., Sugimoto %A K., Hosoki %A M., Nagao %A R., Tokuda %A T., Fujisawa %D 2017 %T Erratum: 1,25-Dihydroxyvitamin D3 Upregulates Functional C-X-C Chemokine Receptor Type 4 Expression in Human Eosinophils %U https://karger.figshare.com/articles/dataset/Erratum_1_25-Dihydroxyvitamin_D_sub_3_sub_Upregulates_Functional_C-X-C_Chemokine_Receptor_Type_4_Expression_in_Human_Eosinophils/5241409 %R 10.6084/m9.figshare.5241409.v1 %2 https://karger.figshare.com/ndownloader/files/8956036 %K 1,25-Dihydroxyvitamin D3/calcitriol %K C-X-C chemokine receptor type 4 %K Chemotaxis %K Eosinophils %X Background: Epidemiological studies suggest that vitamin D may be protective against the inception and exacerbation of allergic diseases. However, the direct effect of vitamin D on eosinophils, the major effector cells in allergic inflammation, is not known. It has been reported that C-X-C chemokine receptor type 4 (CXCR4) in eosinophils is induced in non-Th2 cytokine milieu or in response to glucocorticoids, recruiting the cell to noninflammatory sites. Objectives: To test whether 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3 or calcitriol], the active metabolite of vitamin D, acts directly on eosinophils to induce upregulation of CXCR4. Methods: Peripheral blood eosinophils from normal volunteers were isolated by CD16 immunomagnetic beads. Vitamin D receptor (VDR) expression was detected by RT-PCR. Eosinophils were cultured with 1,25-(OH)2D3 and the survival and expression of CXCR4 on eosinophils were measured by flowcytometry. Eosinophil migration by CXCL-12/SDF-1 in the presence of 1,25-(OH)2D3 was also analyzed. Results: Eosinophils expressed VDR. 1,25-(OH)2D3 prolonged eosinophil survival and upregulated eosinophil surface expression of CXCR4 in a concentration-dependent manner. Interleukin (IL)-5 significantly reduced CXCR4 expression and migration induced by the ligand CXCL-12/SDF-1. 1,25-(OH)2D3 reversed the negative effects of IL-5 on the CXCR4-CXCL12 pathway. Conclusion: 1,25-(OH)2D3 regulates CXCR4 expression in eosinophils. The mechanism may be involved in eosinophil recruitment to noninflammatory sites where the ligand of CXCR4 is constitutively expressed. %I Karger Publishers