title: Splenic tissue autotransplantation in rabbits: no restoration of host defense.
abstract: 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.
  
  
  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.
authors.affiliation: Department of General Surgery, Southeast University, Zhongda Hospital, Nanjing 210009, People's Republic of China. tangwh26@jlonline.com
authors.forename: Wen-hao
authors.initials: WH
authors.lastname: Tang
authors.forename: Fu-le
authors.initials: FL
authors.lastname: Wu
authors.forename: Mao-kui
authors.initials: MK
authors.lastname: Huang
authors.forename: Helmut
authors.initials: H
authors.lastname: Friess
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D007109:Immunity / Q000502:physiology; D007150:Immunohistochemistry; D018655:Lymphocyte Count; D009113:Muramidase / Q000378:metabolism; D016377:Organ Transplantation / Q000379:methods / Q000401:mortality; D011008:Pneumococcal Infections / Q000517:prevention & control*; D011817:Rabbits; D011897:Random Allocation; D012016:Reference Values; D012038:Regeneration / Q000276:immunology*; D012680:Sensitivity and Specificity; D018805:Sepsis / Q000401:mortality / Q000517:prevention & control; D013154:Spleen / Q000502:physiology* / Q000637:transplantation*; D013156:Splenectomy / Q000009:adverse effects / Q000379:methods; D015996:Survival Rate; D014182:Transplantation, Autologous; D016896:Treatment Outcome
chemical_list: D009113:Muramidase