title: Proinflammatory and antiinflammatory cytokine production during ischemia-reperfusion injury in a case of identical twin living donor liver transplantation using no immunosuppression.
abstract: BACKGROUND
  Bolus steroids are usually administered prior to graft reperfusion in an attempt to provide protection against ischemia reperfusion injury (IRI). However, the anti-IRI properties of steroids have not been established. Living donor liver transplantation (LDLT) between identical twins provides a unique opportunity to study the natural production of cytokines during transplantation without the confounding influences of the alloimmune response or of immunosuppression in particular steroids.
  
  
  METHODS
  A 38-year-old male with hepatitis C virus-related cirrhosis and multiple hepatocellular carcinomas received a hepatic right lobe graft from his identical twin. No immunosuppression was administered, not even intraoperative bolus steroids. IRI was assessed by serum transaminases as well as by proinflammatory interleukin (IL) IL-1beta, tumor necrosis factor (TNF)-alpha, IL-8 cytokines and for potent regenerative/anti-inflammatory (IL-6, IL-10) mediators.
  
  
  RESULTS
  Despite no administration of steroids, low peak levels of serum transaminases were observed. Serum IL-6 and IL-10 dramatically and rapidly increased during liver transplantation, namely, 160 and 20 times higher than baseline, respectively. In contrast, IL-1beta and TNF-alpha remained low during and after transplantation and an increase in IL-8 was less obvious.
  
  
  CONCLUSIONS
  Syngeneic LDLT without intraoperative bolus steroids is feasible, yielding no penalty in terms of IRI. A predominance of protective cytokines was observed in the absence of steroids. Thus, the concept that intraoperative administration of steroids is necessary to protect liver transplants from IRI must be revisited.
authors.affiliation: Department of Transplantation and Immunology, Transplant Tolerance Unit, Kyoto University, Faculty of Medicine, Kyoto, Japan.
authors.forename: X
authors.initials: X
authors.lastname: Zhao
authors.forename: T
authors.initials: T
authors.lastname: Koshiba
authors.forename: Y
authors.initials: Y
authors.lastname: Fujimoto
authors.forename: J
authors.initials: J
authors.lastname: Pirenne
authors.forename: A
authors.initials: A
authors.lastname: Yoshizawa
authors.forename: T
authors.initials: T
authors.lastname: Ito
authors.forename: H
authors.initials: H
authors.lastname: Kamei
authors.forename: K
authors.initials: K
authors.lastname: Jobara
authors.forename: K
authors.initials: K
authors.lastname: Ogawa
authors.forename: K
authors.initials: K
authors.lastname: Uryuhara
authors.forename: Y
authors.initials: Y
authors.lastname: Takada
authors.forename: K
authors.initials: K
authors.lastname: Tanaka
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D001219:Aspartate Aminotransferases / Q000097:blood; D006528:Carcinoma, Hepatocellular / Q000601:surgery*; D016207:Cytokines / Q000096:biosynthesis* / Q000097:blood; D006526:Hepatitis C / Q000150:complications* / Q000601:surgery*; D006801:Humans; D007375:Interleukin-1 / Q000097:blood; D016753:Interleukin-10 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D008113:Liver Neoplasms / Q000601:surgery*; D016031:Liver Transplantation / Q000276:immunology* / Q000502:physiology; D008297:Male; D015427:Reperfusion Injury / Q000276:immunology*; D014185:Transplantation, Isogeneic / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014430:Twins, Monozygotic
chemical_list: D016207:Cytokines; D007375:Interleukin-1; D015850:Interleukin-6; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase