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

J Transl Med

Allergy and Clinical Immunology Research Centre, The First Affiliated Hospital of Jinzhou Medical University, No. 2, Section 5, Renmin Street, Guta District, Jinzhou, 121001, Liaoning, People's Republic of China.

Published: May 2017

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 CD14NK1R 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5412038PMC
http://dx.doi.org/10.1186/s12967-017-1196-6DOI Listing

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