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- W4234069155 abstract "In Brief Objective To investigate the precise mechanism by which urinary trypsin inhibitor suppresses cytokine production in the prevention of preterm delivery. Methods In vivo and in vitro studies were performed using ascites and peritoneal macrophages obtained on day 15 of pregnancy from female C3H/HeN mice that had been impregnated by B6D2F1 male mice. Lipopolysaccharide receptor, the intracellular signal transduction system, and nuclear factor-κB level were examined. Results In the in vivo study, we found that urinary trypsin inhibitor ameliorated the deterioration of intraperitoneal conditions induced by lipopolysaccharide (ie, increases in ascitic volume, peritoneal cell count, and tumor necrosis factor-α level) and caused a decrease in the binding of lipopolysaccharide to mouse macrophages. In the in vitro studies, urinary trypsin inhibitor decreased the binding capacity of lipopolysaccharide for its receptor, blocked the intracellular signal transduction induced by lipopolysaccharide, and decreased the nuclear factor-κB level. Increases were induced in the binding capacity of the macrophages for urinary trypsin inhibitor and its incorporation into them in the presence of lipopolysaccharide. Conclusion We postulate that urinary trypsin inhibitor may suppress the production of inflammatory cytokines induced by lipopolysaccharide in mouse peritoneal macrophages through suppression of the lipopolysaccharide receptor, inhibition of the intracellular signal transduction system, and decrease in the nuclear factor-κB level. Urinary trypsin inhibitor suppresses production of inflammatory cytokines induced by lipopolysaccharide in pregnant mouse peritoneal macrophages through suppression of lipopolysaccharide receptor and nuclear factor-B levels." @default.
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- W4234069155 date "1999-01-01" @default.
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- W4234069155 title "Protection Against Preterm Delivery in Mice by Urinary Trypsin Inhibitor" @default.
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- W4234069155 doi "https://doi.org/10.1097/00006250-199901000-00021" @default.
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