Prior studies regarding immune function in bile-duct ligated rats have illustrated blunted immune function. The present study measures natural killer (NK) cell activity. Rats underwent bile duct ligation (BDL) or sham celiotomy (SC) and were sacrificed at 1, 2, and 3 weeks after surgery. Ficoll-Hypaque density centrifugation was used to obtain a purified preparation of splenocytes, NK cell activity was determined by incubating varying concentrations of splenocytes with chromium-labelled YAC-1 tumor cells for 4 hours. Chromium release was measured by a gamma counter and expressed as per cent activity (compared with 100 per cent activity obtained by complete lysis with detergent). The experiments were repeated after preincubation in tissue culture flasks to remove an adherent cell population. NK cell activity was decreased at all spleen cell:target cell ratios studies at 1 week after BDL. At 2 weeks after BDL, NK cell activity was decreased at all but the lowest two concentrations; and 3 weeks after BDL, NK cell activity was decreased only at the highest concentrations used. Separation of an adherent cell fraction restored NK cell activity, This suppression in NK cell activity one week after BDL may account, in part, for the poor response of BDL animals to bacterial and immune challenge, Restoration of activity after removal of an adherent cell fraction suggests that macrophages may be at least partly responsible for this inhibition.

Previous studies have shown impaired immune function in biliary obstruction, and our earlier investigations have demonstrated impaired response to alloantigens in the jaundiced rat host. The present study uses the graft versus host (GVH) popliteal lymph node assay to assess the ability of lymphocytes from bile duct ligated animals to elicit an immune response in normal rats. Female Lewis rats underwent bile duct ligation and transection (BDL) or sham celiotomy. A third group of rats served as normal controls. The animals were killed at intervals from 1 to 6 weeks after surgery, and spleen cell preparations were made. Splenocytes (5 x 10(6)) from BDL, sham celiotomy, or normal control rats were injected into the hind footpads of LBNF(1), hybrid rats. The contralateral hind footpads were injected with media as controls. The popliteal lymph nodes were removed and weighed 7 days after injection. The BDL, rats were clinically jaundiced. GVH response was normal at 1 week and decreased at 2 weeks, remaining depressed through 6 weeks. Contralateral control lymph node weights were similar in all groups. Obstructive jaundice not only impairs host immune defense, but also significantly decreases splenocyte GVH capability

Male Lewis strain rats underwent bile duct ligation and division (BDL), selective hepatic duct ligation (SHL), simple ligation and recanalization (RCN), or sham celiotomy (SC). Unoperated rats served as normal controls (NC). At intervals of 1, 2, and 3 weeks postoperatively, the popliteal lymph node assay was used to study host versus graft (HVG) response. LBN-F1 splenocytes (5 × 106) were injected into the hind foot pads, and the contralateral foot pad was injected with medium as a control. The popliteal lymph nodes were removed and weighed 7 days later. In the BDL group, HVG response was significantly impaired at 1 (BDL, 12,9 ± 5.1 mg; SC, 21.6 ± 2.6; NC, 22.4 ± 9.4; P < 0.005, BDL vs SC or NC), 2 (BDL, 12.6 ± 5.6; SC, 19.1 ± 3.0; NC, 15.8 ± 5.8; P < 0.001, BDL vs SC), and 3 weeks (BDL, 8.9 ± 3,9; SC, 21.7 ± 6.3; NC, 16.7 ± 3.8; P < 0.001, BDL vs SC or NC). SHL did not cause hyperbilirubinemia or impair the HVG response at 2 weeks (SHL, 17.2 ± 4.5; NC, 16.7 ± 7.4). The serum bilirubin was normal 2 and 3 weeks after RCN, and the HVG response was normal in both groups; however, the HVG response was somewhat lower at 2 weeks (RCN, 12.1 ± 2.1) than at 3 weeks (RCN, 18.2 ± 4.4; P ± 0,01, RCN 2 weeks vs RCN 3 weeks). BDL causes significant impairment in the murine response to alloantigens as measured by the popliteal lymph node assay. Preservation of sufficient normally drained hepatic parenchyma to prevent hyperbilirubinemia also preserves the HVG response, as does incomplete obstruction (RCN).