Anti-Allergic Inflammatory Effect of Agarum cribrosum and Its Phlorotannin Component, Trifuhalol A, against the Ovalbumin-Induced Allergic Asthma Model

Author:

Kim Joonki12,Lee Sang Heon1,Zhang Siqi12ORCID,Bong Sim-Kyu1,Kim Aaron Taehwan3ORCID,Lee Hara14,Liu Xiaoyong5,Kim Sang Moo6,Kim Su-Nam12

Affiliation:

1. Natural Products Research Center, Korea Institute of Science and Technology (KIST), Gangneung 25451, Republic of Korea

2. Division of Bio-Medical Science and Technology, KIST School, University of Science and Technology, Seoul 02792, Republic of Korea

3. Department of Food Science, University of Massachusetts, Amherst, MA 01003, USA

4. Department of Dentistry, Gangneung-Wonju National University, Gangneung 25457, Republic of Korea

5. Haizhibao Deutschland GmbH, Heiliggeistgasse, 85354 Freising, Germany

6. Department of Marine Food Science and Technology, Gangneung-Wonju National University, Gangneung 25457, Republic of Korea

Abstract

Asthma is a chronic inflammatory disease involving structural changes to the respiratory system and severe immune responses mediated by allergic cytokines and pro-inflammatory mediators. Agarum cribrosum (AC) is a kind of seaweed which contains a phlorotannin, trifuhalol A. To evaluate its anti-allergic inflammatory effect against asthma, an ovalbumin inhalation-induced mouse asthma model was used. Histologic observations proved that trifuhalol A is minimizing the lung and tracheal structure changes as well as the infiltration of eosinophils and mast cells against ovalbumin inhalation challenge. From the serum and bronchoalveolar lavage fluid, ovalbumin-specific IgE and Th2-specific cytokines, IL-4, -5, and -13, were reduced with trifuhalol A treatment. In addition, IL-1β, IL-6, and TNF-α concentrations in lung homogenate were also significantly reduced via trifuhalol A treatment. Taken together, trifuhalol A, isolated from AC, was able to protect lung and airways from Th2-specific cytokine release, and IgE mediated allergic inflammation as well as the attenuation of IL-1β, IL-6, and TNF-α in lung, which results in the suppression of eosinophils and the mast cells involved asthmatic pathology.

Funder

Ministry of Science, ICT, and Future Planning of Korea under the project of the National Research Foundation of Korea

Korea Institute of Science and Technology (KIST) Research Program

Publisher

MDPI AG

Subject

Microbiology (medical),Molecular Biology,General Medicine,Microbiology

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