Up-regulated expression of substance P in CD8+ T cells and NK1R on monocytes of atopic dermatitis

• Main Authors: Zenan Zhang, Wenjiao Zheng, Hua Xie, Ruonan Chai, Junling Wang, Huiyun Zhang, Shaoheng He
• Format: Article
• Language: English
• Published: BMC 2017-05-01
• Series: Journal of Translational Medicine
• Subjects: Allergen; NK1R; T cell; Substance P
• Online Access: http://link.springer.com/article/10.1186/s12967-017-1196-6

Abstract Background Large numbers of CD8+ T cells were observed in atopic dermatitis (AD) skin, and monocytes from AD patients showed increased prostaglandin E2 production. However, little is known about the expression of substance P (SP) and its receptor NK1R in blood leukocytes of patients with AD. Objective To explore the expression of SP and NK1R in leukocytes of AD and the influence of allergens on SP and NK1R expression. Methods The expression levels of SP and NK1R in patients with AD were examined by flow cytometry, ELISA and a mouse AD model. Results The plasma SP level was 4.9-fold higher in patients with AD than in HC subjects. Both the percentage of SP expression in the population and mean fluorescence intensity (MFI) of SP expression were elevated in CD8+ T cells in the blood of AD patients. However, both the CD14+NK1R+ population and MFI of NK1R expression on CD14+ cells were enhanced in the blood of AD patients. Allergens ASWE, HDME and PPE failed to up-regulate SP expression in CD8+ T cells. However, allergens ASWE and HDME both enhanced NK1R expression on CD14+ blood leukocytes regardless of AD or HC subjects. OVA-sensitized AD mice showed an elevated proportion and MFI of SP-expressing CD8+ T cells in the blood, which agrees with the SP expression situation in human AD blood. Injection of SP into mouse skin did not up-regulate NK1R expression on monocytes. Conclusions An elevated plasma SP level, up-regulated expression of SP and NK1R indicate that the SP/NK1R complex is important in the development of AD. Therefore, SP and NK1R antagonist or blocker agents may help to treat patients with AD. Trial registration Registration number: ChiCTR-BOC-16010279; Registration date: Dec., 28, 2016; retrospectively registered