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目的探索支气管哮喘(简称哮喘)小鼠气道中是否存在长期炎症记忆,肺局部淋巴细胞能否传递炎症记忆。方法97只小鼠按随机数字表法分为哮喘组(A组,50只)、长期组(B组,20只)、长期对照组(C组,6只)、过继转移组(D组,12只,根据转移细胞数再分为D1、D2与D3亚组)、过继转移对照组(E组,6只)和naive小鼠组(F组,3只)。B组与D组中分别有亚组用牛血清白蛋白(BSA)代替卵蛋白(OVA)进行第二轮激发,称为BBSA亚组与DBSA亚组。各组评价病理学,检测肺泡嗜酸粒细胞性炎症强度、支气管肺泡灌洗液(BALF)中的细胞总数、细胞分类计数与白细胞介素5(IL5)水平,并比较B组与A组、D组与A组的炎症反应。A组小鼠末次激发后34d,经支气管肺泡灌洗(BAL)得到的混合细胞(BAL细胞)与去除红细胞的脾细胞,分别进行体外培养、变应原刺激,检测细胞增殖与培养液中的IL5浓度。结果(1)A组小鼠主要表现血管炎、肺泡炎与细支气管炎,BALF中的细胞总数、嗜酸粒细胞数和IL5浓度分别在末次激发后8h、24h、240h达峰值[分别为(22±5)×104/ml、(143±009)×104/ml、(751±529)pg/ml]。B组小鼠在第二轮激发前肺中仍有零星的血管炎与肺泡炎;经第二轮激发后血管炎更严重,肺泡炎约为激发前的3倍(激发前、后的肺泡嗜酸粒细胞性炎症指数之比为2123/714),BALF中的细胞
Objective To explore the existence of long-term inflammatory memory in the airway of bronchial asthma (asthma) mice and whether local lymphocytes of the lung can transmit inflammatory memory. Methods Ninety-seven mice were randomly divided into asthma group (A group, 50 rats), long-term group (B group, 20 rats), long-term control group (C group, 6 rats), adoptive transfer group (D group, 12 mice were divided into D1, D2 and D3 subgroup according to the number of metastatic cells), adoptive transfer control group (E group, 6 mice) and naive mice group (F group, 3 mice). Subgroups in group B and group D were stimulated with bovine serum albumin (BSA) instead of ovalbumin (OVA) for the second round of challenge, which was named as BBSA subgroup and DBSA subgroup. The pathology of each group was evaluated. The intensity of alveolar eosinophilic inflammation, the total number of cells in bronchoalveolar lavage fluid (BALF), the cell count and the level of interleukin 5 (IL5) Inflammatory reaction in group D and group A. 34 days after the last challenge in group A, mixed cells (BAL cells) obtained by bronchoalveolar lavage (BAL) and spleen cells obtained by removing erythrocytes were cultured in vitro and were stimulated with allergens respectively to detect the cell proliferation in culture medium IL5 concentration. Results (1) A group of mice mainly showed vasculitis, alveolitis and bronchiolitis, the total number of cells in BALF, the number of eosinophils and the concentration of IL5 peaked at 8h, 24h and 240h after the last challenge respectively [( 22 ± 5) × 104 / ml, (143 ± 009) × 104 / ml, (751 ± 529) pg / ml]. Group B mice still sporadic vasculitis and alveolitis in the second round of challenge before the second round of challenge; vasculitis after the second round of challenge is more serious, alveolitis about 3 times before excitation (before and after stimulation of alveolar Acidophilus inflammatory index ratio 2123/714), cells in BALF