Suppressive Activity of Histamine H1 Receptor Antagonists, Desloratadine and Levocetirizine, on the Production of Periostin from Nasal Epithelial Cells In vitroMasayo Asano1, Tomomi Mizuyoshi1, Shintaro Ishikawa2, Kazuhito Asano3* and Hitome Kobayashi1
- *Corresponding Author:
- Kazuhito Asano
Division of Physiology, School of Nursing and Rehabilitation Sciences, Showa University
1865 Touka-Ichiba, Midori-ku, Yokohama 226-8555, Japan
Tel: +81 45 985 6538
Fax: +81 45 985 7583
E-mail: [email protected]
Received date: March 23, 2017; Accepted date: April 11, 2017; Published date: April 19, 2017
Citation: Asano M, Mizuyoshi T, Ishikawa S, Asano K, Kobayashi H (2017) Suppressive Activity of Histamine H1 Receptor Antagonists, Desloratadine and Levocetirizine, on the Production of Periostin from Nasal Epithelial Cells In vitro. J Allergy Ther 8:253. doi: 10.4172/2155-6121.1000253
Copyright: © 2017 Asano M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: Periostin, a 90-kDa endogenous extracellular matrix protein, is well known to be involved in the development and persistence of allergic rhinitis. Although histamine H1 receptor antagonists are recommended as first choice of agents in the treatment of allergic rhinitis, the influence of the agents on periostin production is not well understood. The present study was undertaken to examine the influence of histamine H1 receptor antagonists on periostin production from nasal epithelial cells after IL-4 stimulation in vitro.
Methods: Human nasal epithelial cells (HNEpC) at a concentration of 1 × 105 cells/ml were stimulated with 10.0 ng/ml IL-4 in combination with either desloratadine (DLT), loratadine (LT), levocetirizine (LCT) or cetirizine (CT). After 48 h, culture supernatants were collected and assayed for periostin levels by ELISA. The influence of LCT on transcription factor, STAT6, activation and periostin mRNA expression were also examined by ELISA and real-time RT-PCR, respectively.
Results: Treatment of cells with DLT, LT, LCT and CT suppressed the ability of HNEpC to produce periostin in response to IL-4 stimulation in dose-dependent manner. The minimum concentration that caused significant suppression is 0.01 mM for DLT, 0.05 mM for LT, 0.05 mM for LCT and 0.1 mM for CT. Treatment of HNEpC with LCT at more than 0.05 mM also suppressed STAT6 activation and periostin mRNA expression induced by IL-4 stimulation.
Conclusion: The present results strongly suggest that histamine H1 receptor antagonists favorably modify the clinical conditions of allergic rhinitis through the suppression of periostin production from nasal epithelial cells after IL-4 stimulation.