Interaction of cytokines and alveolar cells with Pneumocystis carinii in vitro.
Interaction of cytokines and alveolar cells with Pneumocystis carinii in vitro.
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体外细胞因子和肺泡细胞与卡氏肺孢子虫的相互作用。
DOI：
10.1093/infdis/163.3.611
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Pesanti,EL
中科院分区：
文献类型：
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作者：
Pesanti,EL
虽然细胞免疫功能低下是卡氏肺孢子虫肺炎的主要易感因素，但其机制与细胞免疫监视有关。隆起还没有被定义。当P。大鼠肺泡巨噬细胞由半透膜分离，分泌致死物质顶端。只有当巨噬细胞被干扰素-γ激活时，巨噬细胞才被激活；正常巨噬细胞无效。肺泡II型上皮细胞死亡。无论干扰素-v是否存在。可溶性介质的作用也被测试；重组人肿瘤坏死因子α而不是重组大鼠干扰素-γ或内毒素是直接致死的顶端。卡里尼。当加入抗肿瘤坏死因子血清或抗氧化剂(过氧化氢酶和超氧化物歧化酶)时，这些致死效应就被阻止了。提示肿瘤坏死因子可能是参与活化巨噬细胞杀伤P活性的主要介质。表明肿瘤坏死因子对P。Carinii与氧化应激的诱导有关。
Although deficient cellular immune function is a major predisposing factor in the development ofPneumocystis cariniipneumonia, the mechanisms involved in cellular immune surveillance againstP. cariniihave not been defined. WhenP. cariniiwere separated from rat cells by a semipermeable membrane, alveolar macrophages secreted substances lethal toP. cariniionly when the macrophages were activated by interferon-γ; normal macrophages were ineffective. Type II alveolar epithelial cellscaused death ofP. cariniiwhether or not interferon-vwas present. The effects of soluble mediators also were tested; recombinant human tumor necrosis factor-α (TNF) but not recombinant rat interferon-γ or endotoxinwas directly lethal toP. carinii. These lethal effects were prevented when antiserum to TNF or antioxidants (catalase and superoxide dismutase) were included. These data suggest that TNF maybe a major mediator involved in the killing activity of activated macrophages againstP. cariniiand that TNF's activity againstP. cariniiis related to induction of oxidative stresses.