Increased recovery of surfactant protein A in AIDS-related pneumonia.
Increased recovery of surfactant protein A in AIDS-related pneumonia.
复制标题
艾滋病相关肺炎中表面活性蛋白 A 的恢复增加。
DOI：
10.1164/ajrccm/143.5_pt_1.1072
复制
发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Rose,RM
中科院分区：
文献类型：
--
作者：
Phelps,DS;Rose,RM
卡氏肺孢子虫(PC)呼吸道感染是获得性免疫缺陷综合征(AIDS)临床中最常见的严重机会性感染。导致人类免疫缺陷病毒(HIV)感染患者易患PC感染的因素尚不完全清楚。我们推测，肺泡衬里材料(ALM)的改变可能在艾滋病患者PC感染的发病机制中起一定作用。我们比较了正常、非吸烟志愿者和HIV感染肺炎患者的支气管肺泡灌洗液中ALM的成分。采用双抗体夹心法检测肺炎患者血浆表面活性蛋白A(SP-A)水平，发现肺炎患者SP-A水平明显升高。21例正常非吸烟者的SP-A平均值为1.50±0.25微克/毫升(平均值±扫描电子显微镜)。HIV感染者(n=22)SP-A水平显著升高(P<0.01)，平均为5.23±0.54微克/毫升，以临床病情较重的肺炎患者升高最明显。SP-A的升高似乎不是病原体特有的，因为它也在非PC肺炎病例中观察到。我们还发现，感染艾滋病毒的肺炎患者的总蛋白水平几乎高出五倍。这些研究表明，在HIV相关的PC和非PC感染的病例中，ALM的蛋白质成分与正常明显不同。需要进一步研究以确定这些改变的机制以及它们在艾滋病相关肺炎中的作用(如果有的话)。
Respiratory infection withPneumocystis carinii(PC) is the most frequent serious opportunistic infection in the clinical setting of acquired immunodeficiency syndrome (AIDS). The factors responsible for the predisposition of human immunodeficiency virus (HIV)-infected patients for PC infection are not fully understood. We postulated that changes In the alveolar lining material (ALM) could play a role in the pathogenesis of PC infection in AIDS. We have compared constituents of ALM in bronchoalveolar lavage fluid from normal, nonsmoking volunteers with that of HIV-infected patients with pneumonia. Using an ELISA, we found that surfactant protein A (SP-A) was markedly elevated in the pneumonia patients. Mean SP-A values for the normal nonsmoking individuals (n = 21) were 1.50 ± 0.25 µg/ml (mean ± SEM). SP-A levels in the HIV-infected patients (n = 22) were significantly elevated (p < 0.01) with a mean of 5.23 ± 0.54 µg/ml. This increase was greatest in the patients with more clinically severe pneumonia. The increase in SP-A did not appear to be pathogen-specific as it was also observed in cases of non-PC pneumonia. We also found that total protein levels were nearly five times higher in the HIV-infected pneumonia patients. These studies indicate that the protein component of the ALM is markedly different from normal in cases of HIV-associated PC and non-PC infection. Further investigation is needed to determine the mechanism of these alterations and their role, if any, in AIDS-related pneumonia.