Artigo Revisado por pares

Tussilagone inhibits dendritic cell functions via up-regulating heme oxygenase-1 expression (THER5P.833)

2014; American Association of Immunologists; Volume: 192; Issue: 1_Supplement Linguagem: Inglês

10.4049/jimmunol.192.supp.200.12

ISSN

1550-6606

Autores

Yunsoo Park, Hwa Sun Ryu, Ji Sung Kim, Ju Young Kim, Yong Guk Kim, Min Ji Pyo, Mi Jeong Park, Hong Kyung Lee, Bang Yeon Hwang, Young‐Soo Kim, Sang‐Bae Han,

Tópico(s)

Paraquat toxicity studies and treatments

Resumo

Abstract Sesquiterpenoid tussilagone (TUS) has a variety of pharmacological activities. In this study, the effects of TUS on dendritic cell (DC) functions and the underlying mechanisms were investigated. TUS inhibited lipopolysaccharide (LPS)-induced activation of DCs, which was proved by the decreases of surface molecule expression, cytokine production, antigen uptake, migration, and allogenic T cell activation. TUS inhibited LPS-induced activation of NF-kB, MAPKs, and IRF-3 signalings. However, TUS did not directly inhibit kinase activities of IRAK4, IRAK1, TAK1 and IKK, suggesting that signaling molecules downstream from toll-like receptor (TLR) 4 might not be the direct targets of TUS. Instead, TUS activated heme oxygenase-1 (HO-1), which was a rate-limiting enzyme involved in heme degradation to immunosuppressive products, such as carbon monoxide and biliverdin. HO-1 antagonist reversed the inhibitory activity of TUS in DCs. Taken together, this study suggests that TUS might be an inducer of HO-1, which indirectly inhibits TLR signalings and functional activation of LPS-treated DCs

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