Conclusion
CCR3+ and CD123+HLA-DR- cells are likely involved in AA and AR via SP and NK1R. IgE-related mechanism may participate in upregulation of NK1R expression.
Methods
Expression of SP and NK1R was detected by flow cytometry, NK1R mRNA expression was detected by real time quantitative polymerase chain reaction (qPCR), and mouse AR and AA models were employed for in vivo study.
Purpose
To explore expression of SP and NK1R in basophils of allergic asthma (AA), allergic rhinitis (AR) and AR combined with AA (ARA), and influence of allergens and immunoglobulin E (IgE) mediated mechanisms on SP and NK1R expression.
Results
SP+ and NK1R+ cells increased in CCR3+ and CD123+HLA-DR- granulocytes of AA. PPE elevated proportions of SP+ cells in CCR3+ and CD123+HLA-DR- granulocytes, whereas ASWE and HDME augmented SP+ cells in CD123+HLA-DR- granulocytes of AR and ARA patients. ASWE, HDME and PPE increased proportions of NK1R+ cells in CCR3+ PBMC and CD123+HLA-DR- granulocytes of AR patients. OVA, Der p1, IL-33, IL-37, IgE and SP enhanced NK1R expression on KU812 cells. NK1R expressing basophils were increased in blood of OVA sensitized and challenged AR and AA mice. FcεRI-KO AA mice seemed to have less NK1R+ basophils than WT AA mice in their blood.