BACKGROUND: Estriol causes sensitization of Kupffer cells to lipopolysaccharide (LPS) via mechanisms dependent on gut-derived LPS. Accordingly, this study examines the effect of estriol treatment on nitric oxide (NO) production from Kupffer cells. METHODS: Rats were given estriol (20 mg/kg body weight) intraperitoneally, and Kupffer cells were isolated 24 hr later. Some rats were treated for 4 days with 150 mg/kg/day of polymyxin B and 450 mg/kg/day of neomycin to prevent growth of intestinal bacteria, the primary source of endotoxin in the gastrointestinal tract. After addition of LPS, NO production by Kupffer cell was detected using a fluorescence indicator, DAF-2. RESULTS: Twenty-four hours after estriol administration, LPS-induced NO production by Kupffer cells was enhanced as compared with control Kupffer cells. Sterilization of the gut with antibiotics blocked this enhancement. CONCLUSIONS: Estriol treatment in vivo enhances LPS-induced NO production in Kupffer cells.
BACKGROUND:Estriol causes sensitization of Kupffer cells to lipopolysaccharide (LPS) via mechanisms dependent on gut-derived LPS. Accordingly, this study examines the effect of estriol treatment on nitric oxide (NO) production from Kupffer cells. METHODS:Rats were given estriol (20 mg/kg body weight) intraperitoneally, and Kupffer cells were isolated 24 hr later. Some rats were treated for 4 days with 150 mg/kg/day of polymyxin B and 450 mg/kg/day of neomycin to prevent growth of intestinal bacteria, the primary source of endotoxin in the gastrointestinal tract. After addition of LPS, NO production by Kupffer cell was detected using a fluorescence indicator, DAF-2. RESULTS: Twenty-four hours after estriol administration, LPS-induced NO production by Kupffer cells was enhanced as compared with control Kupffer cells. Sterilization of the gut with antibiotics blocked this enhancement. CONCLUSIONS:Estriol treatment in vivo enhances LPS-induced NO production in Kupffer cells.