1,25-dihydroxyvitamin d3 promotes a sustained lps-induced nf-κb-dependent expression of cd55 in human monocytic thp-1 cells1,25-dihydroxyvitamin d3促进持续lps-induced nf-κb-dependent人类单核细胞的表达cd55 thp-1细胞.pdfVIP
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1,25-dihydroxyvitamin d3 promotes a sustained lps-induced nf-κb-dependent expression of cd55 in human monocytic thp-1 cells1,25-dihydroxyvitamin d3促进持续lps-induced nf-κb-dependent人类单核细胞的表达cd55 thp-1细胞
1,25-Dihydroxyvitamin D3 Promotes a Sustained LPS-
Induced NF-kB-Dependent Expression of CD55 in Human
Monocytic THP-1 Cells
1 1,2 1
Michael G. Izban *, Bogdan J. Nowicki , Stella Nowicki
1 Department of Microbiology and Immunology, Meharry Medical College, Nashville, Tennessee, United States of America, 2 Department of Obstetrics and Gynecology,
Meharry Medical College, Nashville, Tennessee, United States of America
Abstract
The vitamin D3 system imposes immunosuppressive effects on monocytic cells, in part, by inhibiting NF-kB-dependent
expression of proinflammatory mediators. CD55, a cell surface complement regulatory protein that promotes protective and
anti-inflammatory properties, is reportedly an NF-kB target gene transiently induced in monocytic cells by the bacterial
endotoxin LPS. CD55 is elevated on white cells in women experiencing preterm labor (a pathophysiology commonly
associated with bacterial infection) and failure to maintain CD55 was associated with subsequent preterm delivery. We
examined the influence of vitamin D3 signaling on LPS-induced expression of CD55 in human monocytic THP-1 cells using
quantitative PCR, immunoblot, immunohistochemistry, and NF-kB activation pathway inhibitors. Non-NF-kB targets CD14
and CD11b, which modulate bacterial surveillance and eradication, respectively, were also examined. LPS produced a rapid
transient 1.6-fold increase in CD55 mRNA. 1,25-D3 alone did not affect CD55 mRNA expression within the first 48 h.
However, in 1,25-D3 pretreated cells, LPS produced a .4-fold immediate and sustained increase in CD55 mRNA and protein
expression, which was blocked by NF-kB inhibitors. Our results unexpectedly suggest that vitamin D3 signaling may
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