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目的 研究卡氏肺孢子虫肺炎 (PCP)引起的肺泡表面活性蛋白A和D(SP A、SP D)的变化 ,以探讨其在PCP发病机制中的作用和治疗中的意义。方法 采用清洁级SD大鼠每周 2次皮下注射醋酸可的松方法建立PCP模型为实验组 ,并设正常对照组 ,阴性对照组 ,细菌性肺炎组。 8～12周分批处死动物 ,收集支气管肺泡灌洗液 (BALF) ,细胞计数分类 ;采用免疫斑点法测定BALF中SP A、SP D含量。结果 根据实验设计和所诱导模型分组 ,A组 :正常对照组 ,n =6 ,健康SD大鼠 ;B组 :阴性对照组 ,n =6 ,使用醋酸可的松 (CA) 8周以上未发生肺部感染的大鼠 ;C组 :细菌性肺炎组 ,n=11,CA诱导 8周以上发生细菌性肺炎而无其他肺部感染 ;D组 :PCP组 ,n =14,CA诱导 8周以上出现PCP而无其他肺部感染。BALF中SP A含量在PCP为 (45 .1± 2 2 .1) μg/ml,明显高于阴性对照组的 (16 .2± 9.9) μg/ml和细菌性肺炎组的 (16 .2±5 .6 ) μg/ml(P <0 .0 5 ) ,同样SP D相对含量 (2 42 49± 4780灰度值 )明显高于细菌性肺炎组 (11989± 2 75 0灰度值 )和阴性对照组 (13384± 2 887灰度值 ) (P <0 .0 0 1)。结论 PCP引起肺表面活性蛋白A和D的显著升高 ,且该变化较细菌性肺炎明显 ,应在PCP的防治中引起重视
Objective To study the changes of alveolar surfactant protein A and D (SP A, SP D) induced by Pneumocystis carinii pneumonia (PCP) in order to investigate its role in the pathogenesis of PCP and the significance of its treatment. Methods PCP model was established by subcutaneously injecting cortisone acetate twice a week in clean grade SD rats. The normal control group, negative control group and bacterial pneumonia group were established. BALB / c mice were sacrificed at 8-12 weeks, BALF was collected and the cell count was determined. The levels of SP A and SP D in BALF were determined by immunofluorescence staining. The results were grouped according to the experimental design and the induced model. Group A: normal control group, n = 6, healthy SD rats; group B: negative control group, n = 6, did not occur with cortisone acetate (CA) Group C: bacterial pneumonia group, n = 11, bacterial pneumonia was induced more than 8 weeks without any other lung infection in CA group; Group D: PCP group, n = 14, CA induced more than 8 weeks PCP appears without other lung infections. The level of SP A in BALF was significantly higher in PCP than in control (16.2 ± 9.9) μg / ml and bacterial pneumonia 5 .6) μg / ml (P <0.05). Similarly, the relative content of SP D (2 42 49 ± 47 80 gray value) was significantly higher than that of bacterial pneumonia group (11989 ± 2 75 0 gray value) and negative Control group (13384 ± 2 887 gray value) (P <0.001). Conclusions PCP causes a significant increase of pulmonary surfactant protein A and D, and the change is more obvious than bacterial pneumonia, which should be paid more attention in the prevention and treatment of PCP