Abstract

Allergic rhinitis (AR) is a chronic inflammatory condition affecting the nasal mucosa of the upper airways. Herein, we investigated the effects of extracts from Gardenia jasminoides (GJ), a traditional herbal medicine with anti-inflammatory properties, on AR-associated inflammatory responses that cause epithelial damage. We investigated the inhibitory effects of water- and ethanol-extracted GJ (GJW and GJE, respectively) in an ovalbumin-induced AR mouse model and in splenocytes, differentiated Th2 cells, and primary human nasal epithelial cells (HNEpCs). Administering GJW and GJE to ovalbumin-induced AR mice improved clinical symptoms including behavior (sneezing and rubbing), serum cytokine levels, immune cell counts, and histopathological marker levels. Treatment with GJW and GJE reduced the secretion of Th2 cytokines in Th2 cells isolated and differentiated from the splenocytes of these mice. To investigate the underlying molecular mechanisms of AR, we treated IL-4/IL-13-stimulated HNEpCs with GJW and GJE; we found that these extracts significantly reduced the production of mitochondrial reactive oxygen species via the uncoupling protein-2 and periostin, a biomarker of the Th2 inflammatory response. Our results suggest that GJ extracts may potentially serve as therapeutic agents to improve the symptoms of AR by regulating the Th2 inflammatory response of the nasal epithelium.

Highlights

  • Allergic rhinitis (AR) is a chronic inflammatory condition affecting the nasal mucosa of the upper airways

  • reactive oxygen species (ROS) levels were markedly reduced by GJ water (GJW) or GJE after IL-4/IL-13 stimulation of human nasal epithelial cells (HNEpCs). These results show that GJW and GJE inhibit the production of periostin, an important mediator of inflammation, by decreasing mitochondrial ROS production in IL-4/IL-13-treated HNEpCs

  • Our results show that GJW and GJE are effective inhibitors of AR and that they function by significantly reducing inflammatory cell infiltration, Th2 cytokine production, eosinophil migration, mitochondrial ROS production, periostin production, and p38-MAPK/activating transcription factor-2 (ATF2) activation

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Summary

Introduction

Allergic rhinitis (AR) is a chronic inflammatory condition affecting the nasal mucosa of the upper airways. Administering GJW and GJE to ovalbumin-induced AR mice improved clinical symptoms including behavior (sneezing and rubbing), serum cytokine levels, immune cell counts, and histopathological marker levels. The recruitment and activation of eosinophils concomitant with the allergic inflammatory response is regulated by T-helper type 2 (Th2) cells and cytokines, especially interleukin (IL)-4, IL-5, and IL-13 [6,7]. These cellular events trigger the generation of antigen-specific IgE published maps and institutional affiliations

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