Aim:To investigate the mechanism of immunological liver injury induced by bacilleCalmette-Guerin(BCG)plus lipopolysaccharide(LPS).Methods:Mice were in-jected via the tail vein with 125 mg/kg BCG,and 12 d later,the mice were injectedintravenously with different doses of LPS(125,250,or 375 μg/kg).Serum alanineaminotransferase(ALT)activity and liver pathological changes were examined.The expression of tumor necrosis factor(TNF)-α interleukin(IL)-6,lipopolysac-charide binding protein(LBP)and CD14 mRNA,and NF-κB and IκB-α protein inmouse liver at different time points after BCG and LPS injection were measuredusing RT-PCR,immunohistochemistry and Western blotting analysis,respectively.Results:The activity of serum ALT in mice treated with BCG and LPS was signifi-cantly increased.Different degrees of liver injury,such as inflammatory cellinfiltration,spotty necrosis,piecemeal necrosis,even bridging necrosis,could beseen in liver sections from mice after BCG and LPS administration.Furthermore,thelevels of TNF-α and IL-6 mRNA in mouse liver were significantly elevated afteradministration of BCG plus LPS(P<0.05).The levels of LBP and CD14 mRNA inmouse liver were markedly upregulated after treatment with BCG and LPS,andtreatment with BCG alone led to an increase in CD14 InRNA in mouse liver.Finally,immunoreactivity for NF-κB p65 was predominantly detected in hepatocyte nucleifrom mice treated with BCG plus LPS,compared with the normal group.Proteinlevels of IκB-α were strikingly decreased by LPS or BCG plus LPS treatment,compared with the normal group or BCG group.Conclusion:TNF-α and IL-6mRNA were partially involved in early immunological liver injury induced by chal-lenge with small doses of LPS after BCG priming.Upregulation of TNF-α and IL-6 mRNA might be related to increases in LBP and CD 14 mRNA expression andactivation of NF-κB.Furthermore,BCG priming in immunological liver injury mayoccur via upregulation of CD 14 mRNA expression in monon uclear cell infiltrationinto the liver. Aim: To investigate the mechanism of immunological liver injury induced by bacille Calmette-Guerin (BCG) plus lipopolysaccharide (LPS). Methods: Mice were in-jected via the tail vein with 125 mg / kg BCG, and 12 d later, the mice were injectedintravenouslywith different doses of LPS (125,250, or 375 μg / kg) .Serum alanine aminotransferase (ALT) activity and liver pathological changes were examined.The expression of tumor necrosis factor (TNF) -αinterukukin (IL) -6, lipopolysac-charide binding protein (LBP) and CD14 mRNA, and NF-κB and IκB-α protein in mouse liver at different time points after BCG and LPS injection were measuredusing RT-PCR, immunohistochemistry and Western blotting analysis, respectively. Results: The activity of serum ALT in mice treated with BCG and LPS was signifi-cantly increased. Different degrees of liver injury, such as inflammatory cell infiltration, spotty necrosis, piecemeal necrosis, even bridging necrosis, could be seen in liver sections from mice after BCG and LPS administration. more of the levels of TNF-α and IL-6 mRNA in mouse liver were elevated elevated afantiradistration of BCG plus LPS (P <0.05). The levels of LBP and CD14 mRNA inmouse liver were markedly upregulated after treatment with BCG and LPS, and treatment with BCG alone led to an increase in CD14 InRNA in mouse liver. Finaally, immunoreactivity for NF-κB p65 was predominantly detected in hepatocyte nuclei of mice treated with BCG plus LPS, compared with the normal group. Protein levels of IκB-α were strikingly decreased by LPS or BCG plus LPS treatment, compared with the normal group or BCG group. Confluence: TNF-alpha and IL-6 mRNA were partially involved in early immunological liver injury induced by chal-lenge with small doses of LPS after BCG priming. Upregulation of TNF- α and IL-6 mRNA might be related to LBPs and CD 14 mRNA expression and activation of NF-κB.Furthermore, BCG priming in immunological liver injury may be related to upregulation of CD 14 mRNA expression in monon uclear cell infiltration rationintothe liver