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Honokiol inhibits LPS‐induced maturation and inflammatory response of human monocyte‐derived dendritic cells
Author(s) -
Li ChiaYang,
Chao Louis Kuoping,
Wang ShuChi,
Chang HonZu,
Tsai MinLung,
Fang ShihHua,
Liao PeiChun,
Ho ChenLung,
Chen ShuiTein,
Cheng WeiChung,
Chiang ChiShiun,
Kuo YuehHsiung,
Hua KuoFeng,
Hsu Ian C.
Publication year - 2011
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.22576
Subject(s) - cd80 , cd86 , cd11c , cd40 , p38 mitogen activated protein kinases , microbiology and biotechnology , lipopolysaccharide , honokiol , mapk/erk pathway , chemistry , dendritic cell , monocyte , signal transduction , immune system , t cell , immunology , biology , cytotoxic t cell , biochemistry , in vitro , gene , phenotype
Honokiol (HNK) is a phenolic compound isolated from the bark of houpu ( Magnolia officinalis ), a plant widely used in traditional Chinese and Japanese medicine. While substantial evidence indicates that HNK possesses anti‐inflammatory activity, its effect on dendritic cells (DCs) during the inflammatory reaction remains unclear. The present study investigates how HNK affects lipopolysaccharide (LPS)‐stimulated human monocyte‐derived DCs. Our experimental results show that HNK inhibits the inflammatory response of LPS‐induced DCs by (1) suppressing the expression of CD11c, CD40, CD80, CD83, CD86, and MHC‐II on LPS‐activated DCs, (2) reducing the production of TNF‐α, IL‐1β, IL‐6, and IL‐12p70 but increasing the production of IL‐10 and TGF‐β1 by LPS‐activated DCs, (3) inhibiting the LPS‐induced DC‐elicited allogeneic T‐cell proliferation, and (4) shifting the LPS‐induced DC‐driven Th1 response toward a Th2 response. Further, our results show that HNK inhibits the phosphorylation levels of ERK1/2, p38, JNK1/2, IKKα, and IκBα in LPS‐activated DCs. Collectively, the findings show that the anti‐inflammatory actions of HNK on LPS‐induced DCs are associated with the NF‐κB and mitogen‐activated protein kinase (MAPK) signaling pathways. J. Cell. Physiol. 226: 2338–2349, 2011. © 2010 Wiley‐Liss, Inc.