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目的研究T细胞免疫球蛋白-黏蛋白-1(TIM-1)表达对哮喘小鼠气道MUC5AC及Th2细胞因子的作用,探讨气道黏液高分泌的机制。方法30只健康雌性C57BL/6小鼠,按随机数字表法分为正常、哮喘模型组(哮喘组)和哮喘模型+TIM-1抗体处理组(TIM-1抗体组),每组10只。检测小鼠外周血单个核细胞(PBMCs)TIM-1+细胞比例、气道MUC5AC mRNA表达、肺泡灌洗液(BALF)中IL-13、IL-4、IL-5水平及黏液细胞数量和细胞体积的改变。结果 (1)哮喘组及TIM-1抗体组小鼠外周血PBMCs中TIM-1+细胞比例(11.20%,5.11%)均高于正常组(0.64%,P<0.05),且TIM-1抗体组低于哮喘组(P<0.05)。(2)哮喘组及TIM-1抗体小鼠气道黏液细胞MUC5AC mRNA相对表达(17.3±1.4,5.6±0.3)及IL-13[(16.80±0.63)ng/ml,(5.70±0.64)ng/ml]、IL-4[(614.72±117.39)pg/ml,(325.78±86.54)pg/ml]、IL-5[(1 681.13±613.55)pg/ml,(513.42±86.87)pg/ml]水平均高于正常组[1,(1.09±0.25)ng/ml,(17.56±3.01)pg/ml,(30.78±9.67)pg/ml],TIM-1抗体组小鼠上述指标低于哮喘组(P<0.05)。(3)气道MUC5AC及IL-13表达与TIM-1+细胞表达均呈正相关(r1=0.946,P1=0.004;r2=0.984,P2=0.000)。结论哮喘小鼠外周血TIM-1+细胞升高,可致气道黏液过度分泌;抑制TIM-1表达可减少哮喘气道黏液高分泌。调节TIM-1表达有可能成为减少黏液高分泌及治疗哮喘的新途径。
Objective To study the effect of T cell immunoglobulin-mucin-1 (TIM-1) expression on airway MUC5AC and Th2 cytokines in asthmatic mice and to explore the mechanism of airway mucus hypersecretion. Methods Thirty healthy female C57BL / 6 mice were divided into normal asthma model group (asthma group) and TIM-1 antibody treatment group (TIM-1 antibody group) by random number table. The ratio of TIM-1 + cells in PBMCs, the expression of MUC5AC in airways, the levels of IL-13, IL-4 and IL-5 in bronchoalveolar lavage fluid Volume changes. Results (1) The proportion of TIM-1 + cells in PBMCs in asthmatic group and TIM-1 antibody group was significantly higher than that in normal group (11.20%, 5.11%, 0.64%, P <0.05) Group was lower than asthma group (P <0.05). (2) The relative expression of MUC5AC mRNA in asthmatic mice and TIM-1 antibody-treated mice (17.3 ± 1.4,5.6 ± 0.3) and IL-13 [(16.80 ± 0.63) ng / ml], IL-4 [(614.72 ± 117.39) pg / ml, (325.78 ± 86.54) pg / ml], IL-5 [(1881.13 ± 613.55) pg / ml, (513.42 ± 86.87) pg / ml] (1.09 ± 0.25) ng / ml, (17.56 ± 3.01) pg / ml, (30.78 ± 9.67) pg / ml respectively). The indexes of TIM-1 antibody group were lower than those of the asthma group P <0.05). (3) The expressions of MUC5AC and IL-13 in airway were positively correlated with the expression of TIM-1 + cells (r1 = 0.946, P1 = 0.004; r2 = 0.984, P2 = 0.000). Conclusions The increase of TIM-1 + cells in peripheral blood of asthmatic mice can result in over-secretion of airway mucus, and the inhibition of TIM-1 expression can reduce the airway mucus hypersecretion in asthmatic mice. Regulating TIM-1 expression may be a new way to reduce mucus hypersecretion and treat asthma.