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卡氏肺孢子虫肺炎肺表面活性蛋白A和D的变化 |
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group C: bacterial pneumonia (n=11), rats were injected with cortisone acetate over 8 weeks and resulted in bacterial pneumonia without other pathogens isolated; group D (n=14): rats were injected with cortisone acetate during 8～12 weeks and resulted in PCP without other pathogens isolated. During PCP infection, the total cell counts and the percentage of polymorphonuclears (PMNs) in BALF were significantly increased (P<0.01), but were lower than those in the bacterial pneumonia group. The concentration of SP-A of BALF in PCP (45.1 μg/ml±22.1 μg/ml) was significantly increased in comparison with that in negative control group (16.2 μg/ml±9.9 μg/ml, P<0.05) and that in bacterial pneumonia group (6.2 μg/ml±5.6 μg/ml, P<0.001). We also found that the relative content of SP-D was significantly higher in PCP (24 249±4 780 grey values) than that in both negative control (13 384±2 887 grey values, P<0.001) and bacterial pneumonia group (11 989±2 750 grey values, P<0.001). SP-A and SP-D were also higher in moderate to severe group of PCP than those seen in mild group (P<0.01, P<0.001). Conclusion There was obvious increase of SP-A and SP-D in PCP rats, and particularly, the change of which was greater than that in bacterial pneumonia. Therefore, the alteration of SP-A and SP-D may be of implication in the prevention and management of PCP.
【Key words】Pneumocystis carinii pneumonia; Bronchoalveolar lavage fluids; Surfactant protein A, D
卡氏肺孢子虫肺炎(PCP)是艾滋病(AIDS)等免疫损害宿主最常见的呼吸系统感染性疾病［1］，卡氏肺孢子虫(PC)进入肺泡腔与肺泡上皮相互作用，导致肺泡表面衬层发生改变，肺泡腔内充满大量渗出物。表面活性蛋白A和D(Surfactant Protein A、D；SP-A、SP-D)是肺泡腔内大量渗出物中主要的成分之一。SP-A、SP-D是结构相似的糖蛋白，由肺泡clara细胞及Ⅱ型上皮细胞合成分泌，在调节表面活性磷脂代谢及肺防御功能方面起重要作用。近年来有部分研究发现AIDS合并PCP时肺内SP-A、SP-D水平增高。我们应用醋酸可的松(Cortisone Acetate, CA)诱导SD大鼠建立PCP动物模型，研究SP-A、SP-D的变化，并与CA诱导的免疫抑制大鼠的细菌性肺炎、阴性对照组及正常对照比较，以探讨SP-A、SP-D在PCP发病机制中的作用及治疗中的意义。
材料和方法
一、PCP动物模型的建立
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