卡氏肺囊虫肺炎改变肺收集物SP-A和SP-D的表达和分布。

E. Atochina, J. Beck, S. Scanlon, A. M. Preston, M. Beers
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引用次数: 61

摘要

表面活性蛋白SP-A和SP-D是集合蛋白家族的成员,已被证明在肺宿主防御中起重要作用。这两种蛋白选择性结合卡氏肺囊虫(PC)生物体并调节这种病原体与肺泡巨噬细胞的相互作用。我们假设肺收集素SP-A和SP-D的表达和分布被PC肺感染改变。将PC有机体(2 × 10(5))经气管内接种到不需要类固醇进行免疫抑制的C.B-17 scid/scid小鼠中。接种4周后,将支气管肺泡灌洗液(BAL)分成细胞颗粒、大团聚体(LA)和小团聚体(SA)表面活性剂3个部分,分析每个部分表面活性剂成分的表达情况。在未感染小鼠中,发现大部分SP-A(62% +/- 10%)与LA部分的脂质相关,而55% +/- 14%的SP-D分布在SA部分。疏水蛋白SP-B和SP-C均与LA特异性相关。PC感染导致所有表面活性剂成分的表达发生重大变化。PC感染后LA总蛋白含量基本不变(为对照组的115% +/- 18%),SA蛋白含量显著升高(为对照组的240% +/- 18%,P < 0.001)。相比之下,LA的磷脂含量显著降低(为对照组的53% +/- 5%,P <.001),而SA的磷脂含量升高(为对照组的172% +/- 16%,P <.001)。经Western blot检测,PC肺炎(PCP)诱导肺泡SP-D总蛋白升高3倍,主要表现为SA SP-D升高(454% +/- 135%,P < 0.05)。PCP组肺泡SP-A蛋白总含量也增加,因为SA组SP-A含量增加较多(720% +/- 115%,P < 0.05);洛杉矶的SP-A水平没有变化。肺集合表达的增加是选择性的,因为PCP导致LA中SP-B和SP-C的下调(分别为对照组的5% +/- 2%和13% +/- 2%,P < 0.001)。我们得出结论,PCP诱导肺泡收集水平显著升高是因为SA表面活性剂中SP-A和SP-D蛋白的表达和积累增加。
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Pneumocystis carinii pneumonia alters expression and distribution of lung collectins SP-A and SP-D.
Surfactant proteins SP-A and SP-D, members of the collectin family, have been shown to play a significant role in lung host defense. Both proteins selectively bind Pneumocystis carinii (PC) organisms and modulate the interaction of this pathogen with alveolar macrophages. We hypothesized that the expression and distribution of lung collectins SP-A and SP-D is altered by PC lung infection. PC organisms (2 x 10(5)) were inoculated intratracheally into C.B-17 scid/scid mice that do not require steroids for immunosuppression. Four weeks after inoculation, bronchoalveolar lavage (BAL) fluid was fractionated into three fractions-cell pellet, large aggregate (LA), and small aggregate (SA) surfactant-and each fraction was analyzed for the expression of surfactant components. In uninfected mice, the majority of SP-A (62% +/- 10%) was found in association with lipids in the LA fraction, while 55% +/- 14% of SP-D was distributed in the SA fraction. In contrast, both hydrophobic proteins SP-B and SP-C were associated exclusively with LA. PC infection resulted in major changes in the expression of all surfactant components. Total protein content of LA was unchanged by PC infection (115% +/- 18% of control), whereas SA protein content markedly increased (240% +/- 18% of control level, P <.001). In contrast, the phospholipid content of LA was significantly decreased (53% +/- 5% of control level, P <.001), whereas the SA phospholipid content of infected mice was increased (172% +/- 16% of control level, P <.001). By Western blotting, PC pneumonia (PCP) induced a 3-fold increase in the total alveolar SP-D protein that was reflected mainly in increases in SA SP-D (454% +/- 135% of control, P <.05). The total alveolar SP-A protein content was also increased in PCP because of a large increase in SP-A in SA (720% +/- 115% of control, P <.05); SP-A levels in LA were unchanged. The increases in lung collectin expression were selective, because PCP resulted in the down-regulation of both SP-B and SP-C in LA (5% +/- 2% and 13% +/- 2% of control, respectively, P <.001). We conclude that PCP induces marked elevations in alveolar collectin levels because of increased expression and accumulation of SP-A and SP-D protein in SA surfactant.
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