出 处:《中华结核和呼吸杂志》2004年第10期672-677,共6页Chinese Journal of Tuberculosis and Respiratory Diseases
基 金:国家自然科学基金资助项目(39770340)
摘 要: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)。Objective To investigate if long lived inflammatory memory exists in the airway of asthmatic mice, and whether pulmonary local lymphocytes could transfer the inflammatory memory Methods 97 mice were divided into six groups by random number meter: asthma group (group A, n =50), long term group(group B, n =20), control group of long term (group C, n =6), adoptive transfer group (group D, n = 12, subgroups D 1, D 2 and D 3 divided based on the transferred cells counts), adoptive transfer control group(group E, n =6), and naive group( group F, n =3) There were subgroups using BSA(bovine serum album) substituting OVA(ovalbumin) for the second challenge, named subgroup B BSA in group B and subgroup D BSA in group D Pathologic changes, alveolar eosinophil infiltration, total cell counts(TCC) in bronchoalveolar lavage fluid (BALF), leukocyte differentials, and BALF IL 5 level were assayed in every group Comparisons of inflammation responses between group B and group A, also between group D and group A were made From asthmatic mice 34 d post aerosol, bronchoalveolar lavage(BAL) cells and splenocytes free of red blood cells(NR splenocyte in brief) were cultured in vitro and stimulated with allergens, to detect cell proliferations and IL 5 levels in the supernatant Results (1)Vasculitis, alveolitis and bronchiolites were observed in group A TCC, BALF esosinophil and IL 5 reached peak on 240 h and 8 h, 24 h post aerosol respectively [(22±5)×10 4/ml, (1 43±0 09)×10 4/ml and (75 1±52 9)pg/ml, respectively] There were scattered vasculitis and alveolitis in group B before second OVA challenge; and more severe vasculitis and 3 fold higher alveolitis (ratio of alveolar eosinophil inflammation indexes is 21 23/7 14) were observed after second challenge TCC and BALF eosinophils reached peak 24 h post aerosol [(121 5±19 1)×10 4/ml and (12 960±2 040)×10 4/ml respectively], BALF IL 5 reached to its highest level [(50 8±18 5)pg/ml] 48 h post aerosol There were mild vasculitis in group B BSA,while TCC [(5 3±2 1)×10 4/ml] an
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