Trifuhalol A Suppresses Allergic Inflammation through Dual Inhibition of TAK1 and MK2 Mediated by IgE and IL-33open access
- Authors
- Bong, Sim-Kyu; Park, No-June; Lee, Sang Heon; Lee, Jin Woo; Kim, Aaron Taehwan; Liu, Xiaoyong; Kim, Sang Moo; Yang, Min Hye; Kim, Yong Kee; Kim, Su-Nam
- Issue Date
- Sep-2022
- Publisher
- MDPI
- Keywords
- trifuhalol A; allergic inflammation; interleukin-33; immunoglobulin E; degranulation; TGF beta-activated kinase 1; MAPK-activated protein kinase 2
- Citation
- INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.23, no.17, pp 1 - 16
- Pages
- 16
- Journal Title
- INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
- Volume
- 23
- Number
- 17
- Start Page
- 1
- End Page
- 16
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/152488
- DOI
- 10.3390/ijms231710163
- ISSN
- 1661-6596
1422-0067
- Abstract
- The activation and degranulation of immune cells play a pivotal role in allergic inflammation, a pathological condition that includes anaphylaxis, pruritus, and allergic march-related diseases. In this study, trifuhalol A, a phlorotannin isolated from Agarum cribrosum, inhibited the degranulation of immune cells and the biosynthesis of IL-33 and IgE in differentiated B cells and keratinocytes, respectively. Additionally, trifuhalol A suppressed the IL-33 and IgE-mediated activation of RBL-2H3 cells through the regulation of the TAK1 and MK2 pathways. Hence, the effect of trifuhalol A on allergic inflammation was evaluated using a Compound 48/80-induced systemic anaphylaxis mouse model and a house dust mite (HDM)-induced atopic dermatitis (AD) mouse model. Trifuhalol A alleviated anaphylactic death and pruritus, which appeared as an early-phase reaction to allergic inflammation in the Compound 48/80-induced systemic anaphylaxis model. In addition, trifuhalol A improved symptoms such as itching, edema, erythema, and hyperkeratinization in HDM-induced AD mice as a late-phase reaction. Moreover, the expression of IL-33 and thymic stromal lymphopoietin, inflammatory cytokines secreted from activated keratinocytes, was significantly reduced by trifuhalol A administration, resulting in the reduced infiltration of immune cells into the skin and a reduction in the blood levels of IgE and IL-4. In summarizing the above results, these results confirm that trifuhalol A is a potential therapeutic candidate for the regulation of allergic inflammation.
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