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Open Access Open Badges Research article

Early innate immune events induced by prolonged cold ischemia exacerbate allograft vasculopathy

Jennifer J Devitt1*, Chelsey L King2, Timothy DG Lee123 and Camille L Hancock Friesen12

Author Affiliations

1 Department of Surgery, Dalhousie University, 5850 College Street, Halifax, B3H 1X5, Canada

2 Department of Pathology, Dalhousie University, 5850 College Street, Halifax, B3H 1X5, Canada

3 Department of Microbiology & Immunology, Dalhousie University, 5850 College Street, Halifax, B3H 1X5, Canada

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Journal of Cardiothoracic Surgery 2011, 6:2  doi:10.1186/1749-8090-6-2

Published: 6 January 2011



Ischemia/reperfusion induced innate immune injury is inescapable in solid organ transplantation. Prolonged cold ischemia exacerbates the primary manifestation of late graft rejection, allograft vasculopathy (AV). The relationship between prolonged cold ischemia and late graft events is unclear and the subject of this study.


Aortic interposition transplants were performed between fully disparate mice treated with CyclosporineA. Allografts were exposed to 20 min or 60 min of cold ischemia and harvested between 1 d-6 wk. Lesion size, smooth muscle cells (SMC), neutrophils (N∅), and CD8+ T cells were quantified.


Early SMC loss was identical in both groups. When compared to 20 min cold ischemia, grafts exposed to 60 min exhibited greater early N∅ influx, greater SMC proliferation but fewer medial SMC at 1 wk and 2 wk. Subsequently, earlier and greater CD8+ T cell infiltration were seen in the 60 min group with larger lesions at every time point.


These data suggest that the larger neointimal lesions in grafts exposed to 60 min cold ischemia result from enhanced early innate immune events resulting in impaired SMC recovery and subsequent increased adaptive immune response.