Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Wertheim cung cấp cho các bạn kiến thức về ngành y đề tài: Neutrophil mediated smooth muscle cell loss precedes allograft vasculopathy. | King et al. Journal of Cardiothoracic Surgery 2010 5 52 http content 5 1 52 JOURNAL OF CARDIOTHORACIC SURGERY RESEARCH ARTICLE Open Access Neutrophil mediated smooth muscle cell loss precedes allograft vasculopathy Chelsey L King 1 Jennifer J Devitt2 Timothy DG Lee1 2 3 and Camille L Hancock Friesen 1 3 Abstract Background Cardiac allograft vasculopathy AV is a pathological process of vascular remodeling leading to late graft loss following cardiac transplantation. While there is consensus that AV is alloimmune mediated and evidence that the most important alloimmune target is medial smooth muscle cells SMC the role of the innate immune response in the initiation of this disease is still being elucidated. As ischemia reperfusion IR injury plays a pivotal role in the initiation of AV we hypothesize that IR enhances the early innate response to cardiac allografts. Methods Aortic transplants were performed between fully disparate mouse strains C3H HeJ and C57BL 6 in the presence of therapeutic levels of Cyclosporine A as a model for cardiac AV. Neutrophils were depleted from some recipients using anti-PMN serum. Grafts were harvested at 1 2 3 5d and 1 2wk post-transplant. Ultrastructural integrity was examined by transmission electron microscopy. SMC and neutrophils were quantified from histological sections in a blinded manner. Results Grafts exposed to cold ischemia but not transplanted showed no medial SMC loss and normal ultrastructural integrity. In comparison allografts harvested 1d post-transplant exhibited 90 loss of SMC p . SMC partially recovered by 5d but a second loss of SMC was observed at 1wk. SMC loss at 1d and 1wk post-transplant correlated with neutrophil influx. SMC loss was significantly reduced in neutrophil depleted recipients p . Conclusions These novel data show that there is extensive damage to medial SMC at 1 d post-transplant. By depleting neutrophils from recipients it was demonstrated that a portion
