Background: The loss of spleen may increase the incidence of overwhelming sepsis. To prevent this, splenic autotransplantation has been performed in humans and experimental animals. However, there is still controversy about the effectiveness of regenerated splenic tissue in preventing infection. This study explored the effectiveness of splenic tissue autotransplantation in restoring host defense. Materials and methods: Rabbits were divided into three groups: splenic autotransplantation, sham operation, and total splenectomy. Histomorphology, T-lymphocyte count, serum lysozyme levels, hemolysin titers, and pneumococcal clearance were observed as read-out parameters over 24 weeks. Results: Histological study showed that the white pulp was poorly developed and central arterioles were missing in the regenerated splenic tissue of the autotransplanted rabbits. The weight of regenerated spleens recovered 6 months later in the splenic autotransplantation group was 11% of that in the sham operation group and was significantly less than the weight at implantation. There was no significant difference in the number of T lymphocytes or level of serum lysozyme between the three groups. A poor antibody response by the rabbits in the splenic autotransplantation and total splenectomy groups was noted after the primary intravenous administration of sheep red blood cells compared to those of sham operation group. After the challenge with type 3 pneumococci intravenously, pneumococcal clearance from the bloodstream in the splenic autotransplantation group did not differ significantly from that in the total splenectomy group, but was markedly delayed compared with that in the sham operation group. Conclusions: The low quantity and poor quality of the regenerated splenic tissue contribute to the inferior immunoprotective ability of animals autotransplanted with one-third of the original spleen. This suggests that the regenerated spleen cannot compensate for the immunological function of the original one, especially host resistance to infection.

The aim of the present study was to investigate predisposing factors that lead to the formation of gallstones. In a group of 70 patients (51 with gallstones and 19 without, 20 possible risk factors were studied: percent of ideal body weight, the presence of superoxide dismutase in erythrocytes and in serum, lipid peroxide in serum, total serum cholesterol (Ch), high-density lipoprotein (HDL)-cholesterol (Ch), low-density lipoprotein (LDL)-Ch, very low-density lipoprotein (VLDL)-Ch, serum triglyceride (TG), HDL-TG, LDLTG, VLDL-TG, serum bile acids (lithocholic acid, deoxycholic acid, chenodeoxy cholic acid, ursodeoxycholic acid, and cholic acid) and serum apolipoproteins (apo A-l, apo B-]00, and apo A-1/apo B-100). Levels of apo B-100 and serum insulin in patients with gallstones were strikingly higher, and superoxide dismutase in erythrocytes was significantly lower than in individuals with no gallstones. Apo A-1 and HDL-Ch were also higher and LDL-Ch was lower in the gallstone group, albeit non-significantly so (P > 0.05) by t-test. However, Apo A-l, HDL-Ch, and LDL-Ch showed remarkably good discriminatory power in stepwise discriminant analysis of the 20 factors. Bile lipid composition was also measured and the cholesterol saturation index was calculated, but no significant differences were seen between the two groups. The results demonstrate that serum lipid patterns differ to some extent in patients with and without gallstones. Lipid derangement may contribute to the development of gallstone disease.