Pediococcus Pentosaceus from the Sweet Potato Fermented Ger-Minated Brown Rice Can Inhibit Type I Hypersensitivity in RBL-2H3 Cell and BALB/c Mice Models.

Kyu-Ree Dhong,Hye-Jin Park

doi:10.3390/microorganisms9091855

Abstract

In this study, the effect of GBR fermented with the Pediococcus pentosaceus SP024 strain on IgE/Ag mediated passive cutaneous anaphylaxis (PCA) was investigated. Protocatechuic acid and trans-ferulic acid levels in GBR-SP024 increased more than those in unfermented GBR, respec-tively. The inhibitory activity of GBR-SP024 on β-hexosaminidase release and the level of proin-flammatory cytokine mRNA expression (tumor necrosis factor-α (TNF-α) and interleukin 4 (IL-4)) was observed in IgE/Ag-stimulated RBL-2H3 cells. Western blot analysis showed that GBR-SP024 significantly inhibited the phosphorylation of the linker for activation of T cell (LAT) and nuclear factor-κB (NF-κB) in IgE/Ag-stimulated RBL-2H3 cells. Further, we investigated the anti-allergic effect of GBR-SP024 using PCA murine model. The number of infiltrated immune cells and degranulated mast cells in GBR-SP024 treated dermis was lower than that in the GBR-treated mice. In addition, mRNA expression of 5-lipoxygenase (5-LOX) in the dermis of ear tissue declined in the GBR-SP024–treated group, compared to that in the GBR group. GBR-SP024 was also more effective than GBR at reducing the levels of IL-33 protein expression in IgE/Ag-stimulated BALB/c mice. Our study suggests the potential usage of GBR-SP024 as a dietary supplement or an adjuvant for treating IgE-dependent-allergic diseases.

Highlights

Allergic asthma, allergic rhinitis, urticaria, anaphylaxis, and atopic dermatitis are known to be caused by allergic inflammation following IgE-dependent mast cell activation.Since the year 2000, the prevalence of allergic inflammatory diseases has rapidly increased.Approximately 20% or more of the US population currently suffers from allergic rhinitis and atopic dermatitis
Our study suggests the potential usage of germinated brown rice (GBR)-SP024 as a dietary supplement or an adjuvant for treating
GBR-SP024 significantly suppressed the level of phosphorylated linker for activation of T cell (LAT) and nuclear factor-κB (NF-κB) proteins, compared to GBR (p < 0.05). These results suggested that GBR-SP024 showed anti-allergic properties in IgE/Agstimulated RBL-2H3 cells by suppressing the activation of signaling molecules in the

Summary

Introduction

Allergic rhinitis, urticaria, anaphylaxis, and atopic dermatitis are known to be caused by allergic inflammation following IgE-dependent mast cell activation.Since the year 2000, the prevalence of allergic inflammatory diseases has rapidly increased.Approximately 20% or more of the US population currently suffers from allergic rhinitis and atopic dermatitis. Allergic rhinitis, urticaria, anaphylaxis, and atopic dermatitis are known to be caused by allergic inflammation following IgE-dependent mast cell activation. Upon IgE activation, mast cells immediately secrete preformed and newly synthesized mediators such as histamine, leukotrienes, prostaglandins, proteases, and cytokines, giving rise to acute reactions, such as vasodilation and bronchoconstriction [2]. Allergic responses trigger the activation and infiltration of various inflammatory cells, including mast cells and lymphocytes. The rapid release of mediators and cytokines by mast cells is considered to induce and prolong these responses, leading to chronic inflammation [3]. Chronic disease is aggravated by repeated acute responses to ambient factors. Inhibition of the immediate phase reaction is the most important challenge in the treatment of allergic inflammatory diseases [4]

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