目的研究巨噬细胞的极化状态及IL-17在OB发生中的作用。方法采用小鼠同种异体原位气管移植模型模拟闭塞性细支气管炎的病理改变。20~25 g清洁级C57BL/6,雄性,20只;IL-17基因敲除C57BL/6,雄性,10只;BALB/c雄性,10只,按体质量随机配对分为三组。正常C57BL/6(n=10)无手术对照组;实验组A:BALB/c(n=5)→C57BL/6(n=10)组;实验组B:BALB/c(n=5)→IL-17基因敲除C57BL/6(n=10)组。分别于术后第14、30天取出移植气管进行病理形态学检测。于术后第7、14、30天检测脾脏中巨噬细胞M1型巨噬细胞的标记CD86的表达水平。结果与对照组相比,接受气管移植的野生型小鼠中,M1型巨噬细胞的标记CD86随移植后时间的延长,逐渐下调;IL-17基因敲除受体组巨噬细胞表面CD86的表达水平与对照组相比,明显下调。BALB/c→C57BL/6组较对照组管腔明显狭窄,BALB/c→IL-17基因敲除组较BALB/c→C57BL/6组管腔狭窄明显减轻。结论巨噬细胞向M1方向极化与OB发生的病理过程密切相关,IL-17基因敲除明显下调小鼠气管移植模型体内巨噬细胞表面CD86的表达水平,并减轻气管移植物的病理改变。
Objective To investigate the role of macrophage polarization and IL-17 in obliterative bronchiolitis( OB). Methods Pathogen-free male C57BL /6,IL-17-deficient C57BL /6 and BALB / c mice w eighing 20 - 25 g w ere assigned to three groups. The obliterativel bronchiolitis model w as established by orthotopic trachea transplatation. Ten C57BL /6 mice had no operation served as normal controls. Mice in experimental groups A and B received orthotopic trachea transplantation; group A: BALB / c( n = 5) →C57BL /6( n = 10); group B: BALB / c( n = 5) →IL-17-deficient C57BL /6( n = 10). Native and transplanted lungs w ere harvested after 14 d and 30 d,respectively. CD86 expression in macrophages of spleens w as analysed by flow cytometry at the 7 th,14 th and 30 th days after operation. The samples were stained with H-E and examined under light microscopy. Results Compared to group A,CD86 expression in macrophages of group B w as significantly decreased. Furthermore, airw ay obliteration and epithelial destruction in group A w ere significantly attenuated compared w ith those in group B on the 14 th and 28 th days after transplantation. Conclusion IL-17 deficiency can decrease the M1 polarization of macrophages and attenuate the pathological changes of obliteral bronchiolitis in murine model after trachea transplantaion.