Undaria pinnatifida ameliorates nasal inflammation by inhibiting eosinophil and mast cell activation and modulating the NF‐κB/MAPKs signaling pathway

Author:

Yu Zhen Nan1ORCID,Fan Yan Jing12,Nguyen Thi Van1,Piao Chun Hua13,Lee Byung‐Hoo4,Lee So‐Young56,Shin Hee Soon56,Song Chang Ho17,Chai Ok Hee17

Affiliation:

1. Department of Anatomy Jeonbuk National University Medical School Jeonju South Korea

2. Department of Basic Medicine, School of Medicine Liaocheng University Liaocheng Shandong China

3. Department of Pulmonary and Critical Care Medicine Yantai Yuhuangding Hospital Yantai China

4. Department of Food Science and Biotechnology Gachon University Seongnam South Korea

5. Division of Food Functionality Research Korea Food Research Institute Wanju South Korea

6. Division of Food Biotechnology Program Korea University of Science and Technology Daejeon South Korea

7. Institute for Medical Sciences Jeonbuk National University Jeonju South Korea

Abstract

AbstractBackgroundAllergic rhinitis (AR) is the most prevalent form of atopic disease. Undaria pinnatifida has potent antioxidative, antidiabetic, and anti‐inflammatory properties.AimsWe investigated the immunomodulatory effect of Undaria pinnatifida extract (UPE) on allergic inflammation in an AR mouse model.Materials & MethodsMice were sensitized and intranasally challenged with ovalbumin (OVA), and the Th1/Th2 and Th17/Treg‐related cytokines and histopathology were exanimated after UPE treatments. Enzyme‐linked immunosorbent assay was performed using serum samples and NALF to detect OVA‐specific immunoglobulins and inflammatory cytokines. Mitogen‐activated protein kinases (MAPKs) were measured by western blotting analysis, and an in vitro study measured mast cell activation induced by compound 48/80.ResultsAfter UPE treatment, nasal and lung allergy symptoms, nasal mucosal swelling, and goblet cell hyperplasia were ameliorated. Oral UPE regulated the balance of Th1/Th2 and Th17/Treg cell differentiation in AR mice in a dose‐dependent manner. In addition, UPE attenuated the migration of eosinophils and mast cells to the nasal mucosa by suppressing nuclear factor kappa B (NF‐κB)/MAPKs. The levels of anti‐OVA IgE and IgG1 were also decreased.DiscussionUPE inhibited inflammation by regulating the NF‐κB/MAPKs signaling pathway and supressing the activation of critical immune cells such as eosinophils and mast cells.ConclusionUPE may have therapeutic potential for AR.

Funder

Korea Food Research Institute

Publisher

Wiley

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