Neutrophil chemotaxis in bile duct-obstructed rats, and effect of internal biliary drainage.

BACKGROUND/AIMS: Our previous studies demonstrated enhanced neutrophil chemotaxis in bile duct-ligated, obstructive jaundice rats. In the present study, we produced a reversible obstructive jaundice model in rats. The efficacy of the present model in producing sufficient bile flow blockade and subsequent internal biliary drainage was assessed. Furthermore, the effect of internal biliary drainage on neutrophil chemotaxis was evaluated. METHODOLOGY: Bile duct was obstructed with a polyester tape attached with a stainless steel coil. Internal biliary drainage was performed by removing the tape. Rats were subjected to either 10 days' bile duct obstruction or 4 days' bile duct obstruction followed by 6 days' internal biliary drainage. Some animals underwent conventional bile duct ligation and dissection for 4 or 10 days. Neutrophil chemotaxis was evaluated with a modified Boyden method using interleukin-8 (recombinant rat Gro-beta) as chemoattractant. RESULTS: The present technique produced sufficient obstructive jaundice as evidenced by increases in serum alanine aminotransferase and total bilirubin throughout the observation period, the values of which were insignificant with those induced by the conventional method. Internal biliary drainage effectively normalized these values. Similarly, neutrophil chemotaxis was enhanced with both procedures, and increased neutrophil chemotaxis was significantly decreased after drainage. CONCLUSIONS: The present reversible obstructive jaundice method is as efficacious as the conventional method for producing obstructive jaundice, and internal biliary drainage could be readily available. With the present model, neutrophil overactivity in obstructive jaundice was effectively alleviated by internal biliary drainage. The result may support the role of preoperative biliary drainage in the prevention of postoperative septic complications.

Marked increase in number of dendritic cells in autoimmune-prone (NZW x BXSB)F1 mice with age.

Here, we report that the number of CD11c(+)CD3(-) B220(-) cells increases in autoimmune-prone male (NZW x BXSB)F1 (W/BF1) mice with age. The CD11c(+)CD3(-)B220(-) cells from W/BF1 mice show a typical stellate shape and induce the proliferation of T cells. In the CD11c(+)CD3(-)B220(-) cells from W/BF1 mice, CD11b (Mac-1alpha), NK 1.1, and CD95 (Fas) are upregulated in comparison with normal mice, while the expression of CD8alpha, CD117 (c-kit), CD135 (Flk-2/Flt-3), and Sca-1 decreases. There is a significant increase in Flt-3L (FL) mRNA in the bone marrow of W/BF1 mice with age. Moreover, activated hemopoietic cells express high levels of FL. The injection of CD11c(+)CD3(-)B220(-) cells from old W/BF1 mice to young W/BF1 mice transiently induces autoimmune disease (thrombocytopenia). These results suggest that hyperproduction of FL from activated hemopoietic cells induces a dramatic increase in the number of dendritic cells in aged W/BF1 mice, followed by the acceleration of autoimmunity.