ObjectiveTo investigate changes of lipopolysaccharidebinding protein (LBP) and its clinical significance in activation of Kupffer cells (KCs) during endotoxemia.MethodsWistar rat endotoxemia model was established by injection of a dose of LPS (5 mg/kg, Escherichia coli O111∶B4) via the tail vein of rats, then sacrificed 1, 3, 6 and 12 hour respectively. Hepatic tissue was collected to measure LBP mRNA expression by reverse transcritasepolymerase chain reaction (RTPCR). The levels of plasma endotoxins, LBP, TNFα and IL6 were determined. The pathological changes of hepatic tissue were observed under electron microscope.ResultsWhen the levels of plasma LPS elevated, expression of LBP mRNA in hepatic tissue were ber than that in control rats. The levels of plasma LBP, TNFα and IL6 were increased markedly also in rat with endotoxemia when compared with that in control groups (P＜0.01). KCs were seen to be enlarged in size, their surface projections were increased in number, and their cytoplasm was full of phagocytic vacuoles or electron dense phagosomes which indicated active phagocytosis.ConclusionLPS can markedly upregulate LBP mRNA expression in hepatic tissue, the levels of plasma LBP also increased. LBP may be a critical factor of LPS which stimulates KCs to produce and release different proinflammary mediators.
Citation：
TU Bing,GONG Jianping,SHI Yujun,LI Xuhong,LIU Changan,LI Shengwei. Changes of LipopolysaccharideBinding Protein and Its Significance During Endotoxemia. CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY, 2003, 10(4): 355-358. doi:
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- 1. Nanbo A, Nishimura H, Muta T, et al. Lipopolysaccharide stimulates HepG2 human hepatoma cells in the presence of lipopolysaccharidebinding protein via CD14 [Ｊ]. Eur J Biochem,1999; 260(1)∶183.
- 2. Heumann D, Adachi Y, Le Roy D, et al. Role of plasma, lipopolysaccharidebinding protein, and CD14 in response of mouse peritoneal exudate macrophages to endotoxin [Ｊ]. Infect Immun, 2001; 69(1)∶378.
- 3. Gong JP, Wu CX, Liu CA,et al. Intestinal damage mediated by Kupffer cells in rats with endotoxemia [Ｊ]. World J Gastroenterol， 2002; 8(5)∶923.
- 4. Vreugdenhil AC, Dentener MA, Snoek AM, et al. Lipopolysaccharide binding protein and serum amyloid A secretion by human intestinal cells during the acute phase response [Ｊ]. J Immunol,1999; 163(5)∶2792.
- 5. Erwin PJ, Lewis H, Dolan S, et al. Lipopolysaccharide binding protein in acute pancreatitis [Ｊ]. Crit Care Med, 2000; 28(1)∶104.
- 6. Clark JG, Madtes DK, Martin TR, et al. Idiopathic pneumonia after bone marrow transplantation: cytokine activation and lipopolysaccharide amplification in the bronchoalveolar compartment [Ｊ]. Crit Care Med,1999; 27(9)∶1800.
- 7. Le Roy D, Di Padova F, Tees R, et al. Monoclonal antibodies to murine lipopolysaccharide (LPS)binding protein (LBP) protect mice from lethal endotoxemia by blocking either the binding of LPS to LBP or the presentation of LPS/LBP complexes to CD14 [Ｊ]. J Immunol, 1999; 162(12)∶7454.
- 8. Lukkari TA, Jarvelainen HA, Oinonen T, et al. Shortterm ethanol exposure increases the expression of Kupffer cell CD14 receptor and lipopolysaccharide binding protein in rat liver [Ｊ]. Alcohol, 1999; 34(3)∶311.
- 9. Scott MG, Vreugdenhil AC, Buurman WA, et al. Cutting edge: cationic antimicrobial peptides block the binding of lipopolysaccharide (LPS) to LPS binding protein [Ｊ]. J Immunol, 2000; 164(2)∶549.
- 10. Amura CR, Kamel T, Ito N, et al. Differential regulation of lipopolysaccharide (LPS) activation pathways in mouse macrophages by LPSbinding proteins [Ｊ]. J Immunol, 1998; 161(5)∶2552.
- 11. Kitchens RL, Wolfbaue G, Albers JJ, et al. Plasm lipoproteins promote the release of bacterial lipopolysaccharide from the monocyte cell surface [Ｊ]. J Biol Chem, 1999; 274(48)∶34116.
