摘要
目的观察小鼠原位气管移植急性排斥反应中各种炎症因子的表达变化。方法选用近交系C57BL/6和BALB/c小鼠进行原位气管移植;H-E染色观察第7、30天移植气管的组织病理变化,并评价阻塞情况;CBA法检测第7天血清及移植气管中IL-2、IL-4、IL-6、IFN-γ、TNF-α、IL-17和IL-10的浓度变化。结果与同系移植组和正常组比较,异系移植组移植气管内膜明显增厚,气道明显狭窄、阻塞,第7天阻塞最重且有大量中性粒细胞、淋巴细胞浸润,第30天时主要为淋巴细胞浸润伴纤维组织增生;术后第7天,血清IL-6明显升高(P<0.05)IL-10等细胞因子略有升高(P>0.05);移植气管匀浆中IL-2、IL-6、IFN-γ、TNF-α的浓度显著升高(P<0.05),IL-10亦有升高,但差异无统计学意义。结论小鼠原位气管移植可模拟肺移植后OB的气道阻塞性病变;术后第7天,移植物中IL-2、IL-6、IFN-γ、TNF-α等促炎因子升高可能是异系小鼠原位气管移植急性排斥反应发生的因素之一。
Objective To investigate transplantation in mice. Methods the cytokine levels in acute rejection of orthotopic tracheal Orthotopic tracheal transplantations were performed in a syngeneic （C57BL/6-C57BL/6） and allogeneic （BALB/c-to-C57BL/6） setting. The grafts were removed on d7 and d30 after transplant for histological evaluation. IL-2, IL-4, IL-6, IFN-γ, TNF-α, IL-17 and IL-10 levels in serum and graft homogenate were measured by CBA on＇ d7. Results Compared to syngeneic group or normal group, the allografts had luminal thickening significantly, with neutrophils and lymphocytes infiltration, mainly lymphocytes infiltration with fibrous tissue hyperplasia in chronic stage, and the airway obstructions were most severe, then gradually decreased. On the 7th day, the serum IL-6 level was significantly increased in allogeneicgroup （P 〈 0.01 ）, but not for IL-10 and other related cytokines （P 〉 0.05 ）. The concentrations of IL-2, IL-6, IFN-γ and TNF-α increased significantly in homogenates of allogeneic graft （P 〈 0. 01 ） ; but there was no significant difference in concentration of IL-4, IL-10 and IL-17 among three groups （ P 〉 0.05 ）. Conclusion Cytokines IL-2, IL-6, IFN-γ and TNF-α may play a role in acute rejection of mouse orthotopic tracheal transplan-tation and IL-10 and other cytokines may also be involved.
出处
《同济大学学报（医学版）》
CAS
2014年第1期35-39,共5页
Journal of Tongji University(Medical Science)
基金
国家自然科学基金(81273263
81202332)
上海市卫生局项目(20114231)
浦东新区卫生系统领先人才培养计划(PW2011-01)
浦东新区卫生系统心血管病重点学科群(PKzxkq2010-01)
关键词
原位气管移植
急性排斥
炎症因子
白介素-6
肿瘤坏死因子-Α
orthotopic tracheal transplantation
acute rejection
inflammation factor
interleukin 6
mmour necrosis factor α
