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Conference Paper: Induction of long-term liver allograft survival by delayed immunosuppression is dependent on interleukin-10

TitleInduction of long-term liver allograft survival by delayed immunosuppression is dependent on interleukin-10
Authors
Issue Date2006
PublisherMunksgaard International Publishers
Citation
World Transplant Congress 2006, Boston, MA, 22 - 27 July 2006. In American Journal of Transplantation, 2006, v. 6 n. S2, p. 132 Abstract no. 198 How to Cite?
AbstractBackground: A transit increase of plasma IL-10 level was detected duringthe early phase after reperfusion in the patients with liver transplantation.However, the possible mechanism that regulates this transit upregulationof endogenous IL-10 and its potential role in ischemia/reperfusion injuryand immune response remains to be determined. Aim of Study: We aimedto explore the potential role of the transit upregulation of endogenous IL-10 in ischemia/reperfusion injury and long-term survival of liver grafts ina rat orthotopic liver transplantation model. Materials and Methods:Male DA (RT1a) and LEW (RT1l) rats were used as donors and recipients,respectively. Experimental groups included: 1) No treatment (isograft); 2)IL-10 neutralizing antibody (isograft); 3) No treatment (allograft); 4) IL-10 Ab (allograft); 5) FK506 1 mg/kg intramuscular injection (im), Days 0-7 (allograft); 6) FK506, Days 2-7 (allograft); 7) IL-10 Ab combined withFK506, Days 2-7 (allograft); 8) Low dose FK506 (0.1 mg/kg); 9) Low doseFK506 combined with IL-10 recombinant protein (allograft). Plasma levelsof IL-10 were detected by ELISA. Primary culture of tissue lymphocyteswas performed. Foxp3 mRNA and protein expression was determined.Flow cytometry was performed to detect IL-10 expression in tissuemacrophages. Results: Long-term survival was observed in isografts,allografts with FK506 treatment and with low dose FK506 combined withIL-10 protein. However, administration of IL-10 neutralizing antibodysignificantly reduced the long-term survival of isografts, and allograftswith FK506 treatment. Decreased plasma levels of IL-10 were found in thegroups receiving IL-10 Ab and FK506 treatment. Parallel to the destructionof liver graft histology, increased plasma levels of ALT and total bilirubinwere detected in the groups with the treatment of IL-10 Ab during the earlyphase after reperfusion. Administration of IL-10 Ab reduced the expressionof IL-10 in tissue macrophages, and at the same time, downregulated theexpression of Foxp3 in the primarily isolated lymphocytes. Conclusions:The transit upregulation of endogenous IL-10 in liver grafts played animportant role in prevention of ischemia/reperfusion injury and inductionof long-term allograft survival, probably through generation of T regulatorycells.
Persistent Identifierhttp://hdl.handle.net/10722/108535
ISSN
2015 Impact Factor: 5.669
2015 SCImago Journal Rankings: 2.792

 

DC FieldValueLanguage
dc.contributor.authorYang, Zen_HK
dc.contributor.authorLau, CKen_HK
dc.contributor.authorNgai, PPen_HK
dc.contributor.authorHo, DWYen_HK
dc.contributor.authorTam, KHen_HK
dc.contributor.authorLam, CTen_HK
dc.contributor.authorPoon, RTPen_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2010-09-26T00:43:42Z-
dc.date.available2010-09-26T00:43:42Z-
dc.date.issued2006en_HK
dc.identifier.citationWorld Transplant Congress 2006, Boston, MA, 22 - 27 July 2006. In American Journal of Transplantation, 2006, v. 6 n. S2, p. 132 Abstract no. 198-
dc.identifier.issn1600-6135-
dc.identifier.urihttp://hdl.handle.net/10722/108535-
dc.description.abstractBackground: A transit increase of plasma IL-10 level was detected duringthe early phase after reperfusion in the patients with liver transplantation.However, the possible mechanism that regulates this transit upregulationof endogenous IL-10 and its potential role in ischemia/reperfusion injuryand immune response remains to be determined. Aim of Study: We aimedto explore the potential role of the transit upregulation of endogenous IL-10 in ischemia/reperfusion injury and long-term survival of liver grafts ina rat orthotopic liver transplantation model. Materials and Methods:Male DA (RT1a) and LEW (RT1l) rats were used as donors and recipients,respectively. Experimental groups included: 1) No treatment (isograft); 2)IL-10 neutralizing antibody (isograft); 3) No treatment (allograft); 4) IL-10 Ab (allograft); 5) FK506 1 mg/kg intramuscular injection (im), Days 0-7 (allograft); 6) FK506, Days 2-7 (allograft); 7) IL-10 Ab combined withFK506, Days 2-7 (allograft); 8) Low dose FK506 (0.1 mg/kg); 9) Low doseFK506 combined with IL-10 recombinant protein (allograft). Plasma levelsof IL-10 were detected by ELISA. Primary culture of tissue lymphocyteswas performed. Foxp3 mRNA and protein expression was determined.Flow cytometry was performed to detect IL-10 expression in tissuemacrophages. Results: Long-term survival was observed in isografts,allografts with FK506 treatment and with low dose FK506 combined withIL-10 protein. However, administration of IL-10 neutralizing antibodysignificantly reduced the long-term survival of isografts, and allograftswith FK506 treatment. Decreased plasma levels of IL-10 were found in thegroups receiving IL-10 Ab and FK506 treatment. Parallel to the destructionof liver graft histology, increased plasma levels of ALT and total bilirubinwere detected in the groups with the treatment of IL-10 Ab during the earlyphase after reperfusion. Administration of IL-10 Ab reduced the expressionof IL-10 in tissue macrophages, and at the same time, downregulated theexpression of Foxp3 in the primarily isolated lymphocytes. Conclusions:The transit upregulation of endogenous IL-10 in liver grafts played animportant role in prevention of ischemia/reperfusion injury and inductionof long-term allograft survival, probably through generation of T regulatorycells.-
dc.languageengen_HK
dc.publisherMunksgaard International Publishers-
dc.relation.ispartofAmerican Journal of Transplantationen_HK
dc.titleInduction of long-term liver allograft survival by delayed immunosuppression is dependent on interleukin-10en_HK
dc.typeConference_Paperen_HK
dc.identifier.emailYang, Z: zfyang@hkucc.hku.hken_HK
dc.identifier.emailLau, CK: lauck@HKUCC-COM.hku.hken_HK
dc.identifier.emailNgai, PP: ppngai@hotmail.comen_HK
dc.identifier.emailHo, DWY: davidho@HKUCC.hku.hken_HK
dc.identifier.emailTam, KH: chrishku@graduate.hku.hken_HK
dc.identifier.emailLam, CT: sctlam@graduate.hku.hken_HK
dc.identifier.emailPoon, RTP: poontp@hkucc.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityPoon, RTP=rp00446en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1600-6143.2006.01442a.x-
dc.identifier.pmid16939431-
dc.identifier.hkuros119190en_HK

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