Undaria pinnatifida extract attenuates allergic airway inflammation by the modulation of epithelial cell dysfunction and oxidative stress

Author:

Yu Zhen Nan1,Fan Yan Jing2,Nguyen Thi1,Piao Chun Hua3,Lee Byung-Hoo4,Lee So-Young5,Shin Hee Soon4,Song Chang Ho1,Chai Ok Hee1

Affiliation:

1. Jeonbuk National University Medical School

2. Liaocheng University

3. Yantai Yuhuangding Hospital

4. Gachon University

5. Korea Food Research Institute

Abstract

Abstract Background: Combinative allergic rhinitis and asthma syndrome (CARAS) is a novel uniform airway inflammation composed of inflammation in the upper and lower respiratory tracts.Undaria pinnatifida (U. pinnatifida), a brown alga commonly grown in the oceans of East Asia, has long been a part of human diet and medicine. Though U. pinnatifida has been reported to have immunomodulatory, anti-inflammatory, anti-oxidant, anti-diabetic and anti-bacterial activities, its specific effect on combined allergic rhinitis and asthma syndrome (CARAS) has not been clarified. Methods:In this study, the anti-allergic and anti-inflammatory effects of U. pinnatifida extract (UPE) were investigated in a mouse model of ovalbumin (OVA)-induced CARAS. ELISA was performed using serum samples, NALF and BALF to detect OVA-specific immunoglobulins and inflammatory cytokines. In addition, we checked the levels of MAPKs using western blotting, and we checked the levels of E-cadherin and ST2 using immunohistochemistry. Results:The oral administrations of UPE inhibited allergic responses by reducing OVA-specific immunoglobulin levels; accordingly, symptoms in early reactions were also significantly improved. UPE inhibited the accumulation of inflammatory cells in both nasal and bronchoalveolar lavage fluid and tissues. UPE also attenuated the expression of Th2 cytokines (IL-4, IL-5, IL-13) and up-regulated the secretion of Th1 cytokines (IL-12, IFN-γ) in nasal and bronchoalveolar lavage fluid. Furthermore, UPE treatment inhibited the mitogen-activated protein kinase and nuclear factor-kappa B signaling pathway in lung homogenates. Also, UPE treatment protected the epithelium integrity by preventing the epithelial shedding from nasal mucosa. In addition, UPE ameliorated the dysfunction of the nasal epithelial barrier by enhancing antioxidant properties. UPE attenuated epithelial cell damage and thus down-regulated the expression of the inflammatory factor IL-33. Conclusions:These results suggest that UPE may potentially treat CARAS by modulating epithelial cell dysfunction and oxidative stress, thereby attenuating the release of IL-33.

Publisher

Research Square Platform LLC

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