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. Author manuscript; available in PMC: 2015 Mar 1.
Published in final edited form as: Am J Transplant. 2014 Feb 6;14(3):568–579. doi: 10.1111/ajt.12605

Figure 2. Prolonged cold ischemia increases early infiltration of innate and adaptive leukocytes into cardiac allografts.

Figure 2

(A) Groups of 4-5 C57BL/6 recipient mice received syngeneic or complete MHC-mismatched A/J cardiac allografts subjected to 0.5, 4, or 8 h cold ischemia prior to transplantation. Grafts were recovered 48 h post-transplant, digested to prepare single cell suspensions, and graft infiltrating cells were analyzed and quantified by antibody staining and flow cytometry. *p < 0.05, **p < 0.01 (B) Groups of 4-5 C57BL/6 recipient mice received syngeneic isografts subjected to 0.5 or 4 h cold ischemic storage prior to transplantation. Grafts were recovered 48 h post-transplant, whole cell RNA was isolated from graft homogenates, and quantitative real-time PCR was used to measure expression levels of mRNA encoding the indicated cytokines and chemokines. Differences in mRNA are expressed relative to isografts subjected to 0.5 h ischemia. *p < 0.05, **p < 0.01 (C) Groups of 4-6 C57BL/6 recipient mice received complete MHC-mismatched A/J cardiac allografts subjected to 0.5 or 4 h cold ischemia and were treated with 200 μg control rat IgG or with 500 μg anti-TNFα mAb on day 0 or 100 μg anti-IL-6 mAb on days 0 and 1 post-transplant. Graft infiltrating cells were quantified 48 h post-transplant. *p < 0.05, **p < 0.01