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

Abstract

Allergic rhinitis (AR) is the most prevalent form of atopic disease. Undaria pinnatifida has potent antioxidative, antidiabetic, and anti-inflammatory properties. We investigated the immunomodulatory effect of Undaria pinnatifida extract (UPE) on allergic inflammation in an AR mouse model. Mice 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. After 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. UPE inhibited inflammation by regulating the NF-κB/MAPKs signaling pathway and supressing the activation of critical immune cells such as eosinophils and mast cells. UPE may have therapeutic potential for AR.