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Triptolide suppresses interleukin-1ß-induced human ß-defensin-2 mRNA expression through inhibition of transcriptional activation of NF-κB in A549 cells

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Affiliated Author(s)
장병철박종구서민호서성일문교철배재훈신동훈
Alternative Author(s)
Jang, Byeong ChurlPark, Jong GuSuh, Min HoSuh, Seong IlMun, Kyo CheolBae, Jae HoonShin, Dong Hoon
Journal Title
International Journal of Molecular Medicine
ISSN
1107-3756
Issued Date
2007
Abstract
. The immunosuppressive effect of triptolide has been
associated with suppression of T-cell activation. However, the
immunosuppressive effects of triptolide on innate immunity
in the epithelial barrier remain to be elucidated. Human ßdefensin
(HBD)-2 is an inducible antimicrobial peptide and
plays an important role in the innate immunity. We have
previously demonstrated that IL-1ß induced HBD-2 mRNA
expression in A549 cells through activation of nuclear factor-
κB (NF-κB) transcriptional factor as well as p38 mitogenactivated
protein kinase (MAPK), c-Jun N-terminal kinase
(JNK), or phosphatidylinositol-3-kinase (PI3K). In this study,
we investigated effects of triptolide on IL-1ß-induced HBD-2
mRNA expression in A549 cells. Triptolide inhibited IL-1ßinduced
HBD-2 mRNA expression in a dose-dependent
manner. Addition of triptolide did not suppress activation of
p38 MAPK, JNK, or PI3K in response to IL-1ß. Triptolide
inhibited IL-1ß-induced MAPK phosphatase-1 expression at
the transcriptional level and resulted in sustained phosphorylation
of JNK or p38 MAPK, explaining the little effect of
triptolide on IL-1ß-induced phosphorylation of these kinases.
Although triptolide partially suppressed IL-1ß-mediated
degradation of IκB-· and nuclear translocation of p65 NF-κB,
triptolide potently inhibited NF-κB promoter-driven luciferase
activity in A549 cells. These results collectively suggest that
the inhibitory effect of triptolide on IL-1ß-induced HBD-2
mRNA expression in A549 cells seems to be at least in part
mediated through nuclear inhibition of NF-κB transcriptional
activity, but not inhibition of p38 MAPK, JNK, or PI3K. This
inhibition may explain the ability of triptolide to diminish
innate immune response.
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