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首页> 外文期刊>Infection and immunity >Enhanced Lung Injury and Delayed Clearance of Pneumocystis carinii in Surfactant Protein A-Deficient Mice: Attenuation of Cytokine Responses and Reactive Oxygen-Nitrogen Species
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Enhanced Lung Injury and Delayed Clearance of Pneumocystis carinii in Surfactant Protein A-Deficient Mice: Attenuation of Cytokine Responses and Reactive Oxygen-Nitrogen Species

机译：表面活性蛋白A缺陷型小鼠肺损伤的增强和卡氏肺孢子虫的清除延迟：细胞因子反应和活性氧氮物种的减弱

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Surfactant protein A (SP-A), a member of the collectin family, selectively binds to Pneumocystis carinii and mediates interactions between pathogen and host alveolar macrophages in vitro. To test the hypothesis that mice lacking SP-A have delayed clearance of Pneumocystis organisms and enhanced lung injury, wild-type C57BL/6 (WT) and SP-A-deficient mice (SP-A?/?) with or without selective CD4+-T-cell depletion were intratracheally inoculated with Pneumocystis organisms. Four weeks later, CD4-depleted SP-A-deficient mice had developed a more severe Pneumocystis infection than CD4-depleted WT (P. carinii pneumonia [PCP] scores of 3 versus 2, respectively). Whereas all non-CD4-depleted WT mice were free of PCP, intact SP-A?/? mice also had evidence of increased organism burden. Pneumocystis infection in SP-A-deficient mice was associated histologically with enhanced peribronchial and/or perivascular cellularity (score of 4 versus 2, SP-A?/? versus C57BL/6 mice, respectively) and a corresponding increase in bronchoalveolar lavage (BAL) cell counts. Increases in SP-D content, gamma interferon, interleukin-4, interleukin-5, and tumor necrosis factor alpha in BAL fluid occurred but were attenuated in PCP-infected SP-A?/? mice compared to WT mice. There were increases in total BAL NO levels in both infected groups, but nitrite levels were higher in SP-A?/? mice, indicating a reduction in production of higher oxides of nitrogen that was also reflected in lower levels of 3-nitrotyrosine staining in the SP-A?/? group. We conclude that despite increases in inflammatory cells, SP-A-deficient mice infected with P. carinii exhibit an enhanced susceptibility to the organism and attenuated production of proinflammatory cytokines and reactive oxygen-nitrogen species. These data support the concept that SP-A is a local effector molecule in the lung host defense against P. carinii in vivo.
机译：表面活性蛋白A（SP-A）是collectin家族的成员，可选择性地与卡氏肺孢子虫结合，并介导病原体与宿主肺泡巨噬细胞之间的相互作用。为了检验以下假设：缺乏SP-A的小鼠延迟了肺孢菌生物的清除并增强了肺损伤，我们使用了野生型C57BL / 6（WT）和SP-A缺陷小鼠（SP-A ？/？）选择性或无选择性CD4 + -T细胞耗竭的气管内接种了肺孢子虫生物。四周后，缺乏CD4的SP-A缺陷小鼠比患有CD4的野生型（卡氏疟原虫肺炎[PCP]评分为3）出现了更严重的肺孢囊菌感染与2）。尽管所有未消耗CD4的野生型小鼠都没有PCP，但完整的SP-A ？/？小鼠也有增加机体负担的证据。 SP-A缺陷小鼠中的肺气肿感染在组织学上与支气管周和/或血管周细胞增多有关（得分分别为4分和2分，SP-A ？/？与C57BL /分别为6只小鼠）和相应的支气管肺泡灌洗（BAL）细胞计数增加。与BAL液相比，SP-D含量，γ干扰素，白细胞介素4，白细胞介素5和肿瘤坏死因子α升高，但与PCP感染的SP-A ？/？小鼠相比，它们减弱了WT小鼠。两个感染组的总BAL NO水平均升高，但SP-A ？/？小鼠的亚硝酸盐水平更高，这表明较高氮氧化物的产生减少也反映在较低水平SP-A ？/？组的3-硝基酪氨酸染色水平我们得出的结论是，尽管炎症细胞增加，但感染了 P的SP-A缺陷型小鼠。 Carinii 对生物体的敏感性增强，促炎细胞因子和活性氧氮物质的产生减弱。这些数据支持了SP-A是肺宿主抗 P的局部效应分子的概念。 Carinii 体内。

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