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2007 ; 1
(ä): 295-302
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Current status of monocyte differentiation-inducing (MDI) factors derived from
human fetal membrane chorion cells undergoing apoptosis after influenza virus
infection
#MMPMID19936095
Uchide N
; Toyoda H
Gene Regul Syst Bio
2007[Nov]; 1
(ä): 295-302
PMID19936095
show ga
Influenza virus infection induces apoptosis and the expression of a set of
pro-inflammatory cytokine genes, such as interleukin (IL)-6, tumor necrosis
factor (TNF)-alpha, interferon (IFN)-beta and IFN-gamma, in cultured human fetal
membrane chorion cells. Monocyte differentiation-inducing (MDI) activity in
culture supernatants is simultaneously increased by the virus infection. The MDI
activity is predominantly influenced by IL-6 molecule in culture supernatants,
and partly by TNF-alpha and IFN-beta, but not IFN-gamma, molecules. The MDI
factors are able to induce the mRNA expression of macrophage class A scavenger
receptor (SR-A), which is one of adhesion and apoptotic cell-recognizing
molecules, and gp91(phox), which is a catalytic subunit of reduced nicotinamide
adenine dinucleotide phosphate (NADPH) oxidase enzyme complex, on monocytic
cells. As a result, monocytes are initiated to differentiate into well-matured
macrophages capable of adhering and producing superoxide through NADPH oxidase.
The matured macrophages, obtained from human monocytic leukemia THP-1 cells by
the treatment with MDI factors, phagocytose apoptotic chorion cell debris
resulting from the virus infection. Subsequent to phagocytosis, an abrupt
increase of superoxide production by macrophages may occur. In this article, we
summarize recent knowledge about the MDI factors derived from human fetal
membrane chorion cells undergoing apoptosis after influenza virus infection, and
discuss their possible pathological roles during pregnancy.