摘要
目的探讨肝脏间质树突状细胞在多器官功能障碍综合征（MODS）免疫紊乱机制中的影响与作用。方法150只C57BL／6小鼠经腹腔注射酵母多糖复制MODS模型，随机分为正常对照组和致伤后3～6h、12～48h、5～7d及10～12d组。观察各组小鼠肝脏间质树突状细胞的形态学变化及其表面标记物CD11c、CD205、CD80和I—A^B的表达水平；用流式细胞术检测各组外周血CD4^＋与CD8^＋的T细胞数量及CD4’／CD8’比值。结果急性损伤期（12～48h）肝脏间质树突状细胞大量增生，CD11c、CD205、CD80和I—A^b表达均较正常对照组显著上升（P均〈0．01），外周血T细胞CD4^＋／CD8^＋比值则明显下降（P〈O．01）；功能衰竭期（10～12d）肝脏间质树突状细胞继续增生，但CD205、CD80和I—A^b表达较急性损伤期显著减少（P〈0．05或P〈0．01），外周血T细胞CD4^-／CD8^＋比值下降至最低。结论肝脏间质树突状细胞参与并影响了MODS中肝脏局部与全身免疫失衡及免疫抑制过程。
Objective To explore the role of liver interstitial dendritic cells in immunodissonance mechanism in multiple organ dysfunction syndrome （MODS）. Methods The model of MODS was replicated by intraperitoneal zymosan injection in C57BL/6 mice. One hundred and fifty mice were randomly divided into groups of normal, 3 - 6 hours, 12 - 48 hours, 5 - 7 days and 10 - 12 days after zymosan injection. Morphological changes in liver interstitial dendritic cells were observed with light and transmission electron microscope. Specific surface markers CD205 and CD1 lc, costimulatory molecules CD80 and I- A^b, CD4^＋, CD8^＋ T lymphocyte subgroups and ratio of CD4^-/CD8^＋ in peripheral blood were detected by immunohistochemistry and flow cytometry. Results In early stage of the challenge, liver interstitial dendritic cells showed a proliferation expressing markers CD80 and I - A^b in a low level. The ratio of CD4^＋/CD8^＋ declined in peripheral blood. In acute stage （12- 48 hours）, interstitial dendritic cells had a continuous proliferation with high expression of CD11c, CD205, CD80 and I -A^b （all P〈0.01 ） and the ratio of CD4^＋/CD8^＋ also declined markedly in peripheral blood as compared with the normal group （P〈0.01）. In function failure stage （10 - 12 days）, interstitial dendritic cells further proliferated, but the expression of CD205, CD80 and I - A^b declined to a very low level, with comparison to that in acute stage （P〈0.05 or P〈0.01）, and the ratio of CD4^＋/CD8^＋ declined remarkably in peripheral blood. Conclusion Liver interstitial dendritic cells participated and influenced the course of dysfunction and suppression of immunity in MODS.
出处
《中国危重病急救医学》
CAS
CSCD
北大核心
2007年第10期596-599,I0002,共5页
Chinese Critical Care Medicine
基金
全军“十五”医学科研基金资助项目（01MA210）
