2011 - ISBTS 2011 Symposium
Oral Communications 2: Ischemia / Reperfusion
4.114 - Influence of ischemic preconditioning on local and systemic humoral and inflammatory indices after intestinal transplantation
Presenter: Ricardo, Camprodon, London, United Kingdom
Authors: Ricardo Camprodon1, Matthew Bowles2, Graham Pockley1
Influence of ischemic preconditioning on local and systemic humoral and inflammatory indices after intestinal transplantation
Ricardo Camprodon1, Matthew Bowles2, Graham Pockley1
1Medical School, Sheffield University, Sheffield, United Kingdom; 2Department of Surgery, Derriford Hospital, Plymouth, United Kingdom
Introduction: Ischemia/reperfusion injury (IRI) promotes acute intestinal graft rejection and effective approaches for protecting intestinal grafts are required. Ischemic pre-conditioning (IPc) ameliorates the deleterious effects of IRI and cold preservation and it might also influence graft rejection.
Aims: To determine the influence of graft IPc on alloantibody (AlloAb) levels, the deposition of immunoglobulins in graft tissue, the induction of stress protein (Hsp60, Hsp70) and ICAM-1 expression in graft tissue and serum Hsp60 and Hsp70 antibody levels.
Methodology: Lewis rats received full-length pre-conditioned or non-pre-conditioned heterotopic Brown Norway intestinal allografts. Isografts acted as controls. Blood and graft tissue were collected pre-sacrifice. Tissue Hsp60, Hsp70 and ICAM-1 expression and IgG1, IgG2 and IgM deposition were determined by immunohistochemistry. Area of staining (mm2) was quantified using image analysis. Serum IgG1, IgG2 and IgM binding to donor CD3+ T cells was determined by flow cytometry and the intensity of staining (FI) used as a measure of MHC class I-specific AlloAbs. Serum Hsp60 and Hsp70 antibodies were determined by ELISA.
Results: (1) Rejection induced IgG1, IgG2 and IgM AlloAbs, and IPc decreased circulating levels of donor-specific IgG1 (FI: 90 vs 75) and intragraft deposition of IgG1 (0.21 v 0.17 mm2). (2) There was a significant linear correlation between tissue and serum levels of IgG1 AlloAbs. (3) IPc attenuated rejection-induced tissue expression of Hsp60 and Hsp70 (Hsp60: 0.65 v 0.95 mm2, Hsp70: 0.65 v 1.15 mm2) and this expression was inversely proportional to serum IgG1 and IgG2 Hsp60 and Hsp70 antibody levels. (4) ICAM-1 expression was significantly lower in IPc grafts (1.05 v 2.06 mm2).
Conclusions: IPc ameliorates anti-graft humoral responses and might protect intestinal allografts. Serum AlloAb measurements could be a useful index of AlloAb-mediated rejection. The reduction in ICAM-1 expression induced by IPc might suggest an effect on the cellular response to intestinal allografts.
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