Mediators of Inflammation
Volume 2014 (2014), Article ID 746846, 13 pages
http://dx.doi.org/10.1155/2014/746846
Research Article
1Department of Otolaryngology, Guangzhou Women and Children’s Medical Center, Guangzhou Medical College, No. 9 Jinsui Road, Guangzhou 510623, China
2Department of Otolaryngology, Head and Neck Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, No. 1665 Kongjiang Road, Shanghai 200092, China
2Department of Otolaryngology, Head and Neck Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, No. 1665 Kongjiang Road, Shanghai 200092, China
Received 9 December 2013; Revised 4 July 2014; Accepted 14 July 2014; Published 11 August 2014
Academic Editor: Arkadiusz Orzechowski
Copyright © 2014 Wenlong Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Background. Interleukin-37 (IL-37), a newly described member of IL-1family, functioned as a fundamental inhibitor of innate inflammatory and immune responses, especially its isoform IL-37b. Objective. This study was undertaken to evaluate the expression and regulation of IL-37b in children with allergic rhinitis (AR).Methods. Forty children with AR and twenty-five normal controls were included. The relationship between IL-37b and Th1/2 cytokines production in serum and nasal lavage was examined by enzyme-linked immunosorbent assay (ELISA). Peripheral blood mononuclear cells (PBMCs) were purified for in vitro regulation experiment of IL-37b. Intranasal mometasone furoate was given in AR children and IL-37b change after one-month treatment was detected using ELISA. Results. We observed significantly decreased IL-37b expression levels in both serum and nasal lavage compared to controls. IL-37b was negatively correlated with Th2 cytokines. Our results also showed that IL-37b downregulated Th2 cytokine expressed by PBMCs and this modulation was through mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K) pathway. We also found that intranasal mometasone furoate therapy can promote nasal IL-37b expression.Conclusion. IL-37b may be involved in Th2 cytokine regulation in AR and its expression was related to the efficacy of intranasal steroid therapy.
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