title: Suppression of acute rejective response following orthotopic liver transplantation in experimental rats infected with Echinococcus multilocularis.
abstract: BACKGROUND
  Hepatic alveolar echinococcosis (AE) is a parasitic disease in humans and caused by the Echinococcus multilocularis (Em). Orthotopic liver transplantation (OLT) may be the only effective treatment for end-stage hepatic AE. However, in some AE patients, extrahepatic Em can not be completely eliminated after OLT. We aimed to study whether the immunological changes caused by Em evasion may influence the rejective response.
  
  
  METHODS
  Rat modles of AE were established by injecting the Em suspension into abdomen of Brown Norway (BN) rats. Three months later, in the experimental group, the liver was transplanted from Lewis (LEW) rats to Em-infected BN rats. In the control group, transplantation was from LEW rats to healthy BN rats. Liver tissue and peripheral blood (PB) samples were collected on days 1, 3, 5, and 7 after OLT. Liver tissue was analyzed after hematoxylin and eosin (H&E) staining; numbers of CD4, CD8, and CD28 on peripheral blood cells were detected by flow cytometry; and expression of the chemokine fractalkine (Fkn) was detected by reverse transcription PCR (RT-PCR). Interleukin-10 (IL-10) was measured in the serum by enzyme-linked immunosorbent assay (ELISA). In every group, eight BN rats were retained for observing survival time.
  
  
  RESULTS
  The survival times of recipients in the experimental group were prolonged compared with those in the control group. The rejective response occurred later and was milder in the experimental group. percentage of CD4, CD8, CD28 T-cells and Fkn mRNA expression were lower in the experimental group. While the serum IL-10 levels were higher in the experimental group than those in the control group.
  
  
  CONCLUSIONS
  Acute rejective response after OLT was attenuated in the rats with Em infection, and the recipients` survival time was prolonged. Em may play a role in this process by elevating IL-10 secretion, decreasing the effector T cells, inhibiting the expression of Fkn, which lead to reduce the inflammatory cells infiltration into the liver.
authors: State Key Lab Breeding of Xinjiang Major Disease Research, First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang 830054, China.
authors: Tao
authors: T
authors: Li
authors: Jin-Ming
authors: JM
authors: Zhao
authors: Yan
authors: Y
authors: Zhang
authors: Zu-la
authors: ZL
authors: Pai
authors: Wei
authors: W
authors: Zhang
authors: Tuer-Hongjiang
authors: TH
authors: Tuxun
authors: Lei
authors: L
authors: Bai
authors: Jiang
authors: J
authors: Wu
authors: Hao
authors: H
authors: Wen
mesh_terms: D000818:Animals; D018106:CD28 Antigens / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes / Q000378:metabolism; D004444:Echinococcosis, Hepatic / Q000401:mortality / Q000601:surgery* / Q000628:therapy*; D048210:Echinococcus multilocularis / Q000472:pathogenicity*; D004797:Enzyme-Linked Immunosorbent Assay; D005434:Flow Cytometry; D006084:Graft Rejection / Q000276:immunology; D016753:Interleukin-10 / Q000097:blood; D016031:Liver Transplantation / Q000009:adverse effects*; D051381:Rats; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D018106:CD28 Antigens; D016753:Interleukin-10