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Abstract
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.
Highlights
The past influenza pandemics clearly demonstrate that influenza virus infection during pregnancy has been implicated as one of the causes of premature delivery, abortion and stillbirth (Hardy et al 1961; Harris, 1919)
We reported that influenza virus replicates in both cultured chorion and amnion cells, while in only chorion cells the virus infection induces apoptosis and the expression of a set of pro-inflammatory cytokine genes, such as interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, interferon (IFN)-β and IFN-γ (Uchide et al 2002a, 2002b)
On the basis of these results, we have suggested that fetal membrane chorion cells play a pivotal role in the pathogenesis of pregnancyassociated complications during intrauterine influenza virus infection through the induction of apoptosis and pro-inflammatory cytokine gene expression (Uchide et al 2005a)
Summary
The past influenza pandemics clearly demonstrate that influenza virus infection during pregnancy has been implicated as one of the causes of premature delivery, abortion and stillbirth (Hardy et al 1961; Harris, 1919). To elucidate the virulence of influenza virus infection to human fetal membranes, we have been investigating the induction of apoptosis and pro-inflammatory cytokine gene expression in primary cultured chorion and amnion cells. On the basis of these results, we have suggested that fetal membrane chorion cells play a pivotal role in the pathogenesis of pregnancyassociated complications during intrauterine influenza virus infection through the induction of apoptosis and pro-inflammatory cytokine gene expression (Uchide et al 2005a).
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