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首页> 外文期刊>Journal of Parasitology >EX VIVO AND IN VITRO IMPAIRMENT OF CD36 EXPRESSION AND TUMOR NECROSIS FACTOR-α PRODUCTION IN HUMAN MONOCYTES IN RESPONSE TO PLASMODIUM FALCIPARUM–PARASITIZED ERYTHROCYTES
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EX VIVO AND IN VITRO IMPAIRMENT OF CD36 EXPRESSION AND TUMOR NECROSIS FACTOR-α PRODUCTION IN HUMAN MONOCYTES IN RESPONSE TO PLASMODIUM FALCIPARUM–PARASITIZED ERYTHROCYTES

机译：对恶性疟原虫寄生性红细胞的反应，人类单核细胞CD36表达和肿瘤坏死因子-α产生的体外和体外损伤

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Severe malaria is associated with the failure of host defenses to control parasite replication, with the excessive secretion of proinflammatory cytokines such as tumor necrosis factor–α (TNF-α), and with the sequestration of parasitized erythrocytes (PEs) in the microcirculation of vital organs. The scavenger receptor CD36, known as a major sequestration receptor, has also been identified as an important factor in mediating nonopsonic phagocytosis of PEs by monocytes and macrophages. The specific consequence of this phagocytosis is a decrease in parasite-induced TNF-α secretion. We evaluated the variations in CD36 level and in lipopolysaccharide (LPS)-induced TNF-α production in monocytes from Plasmodium falciparum–infected patients and in vitro in the presence of PEs. Both the monocytes from infected patients and from in vitro culture showed a decrease of CD36 expression and a reduced production of TNF-α induced by LPS. Using incubation assays with no contact between monocytes and PEs, or in the presence of a soluble supernatant obtained from the incubation of monocytes and PEs, this study shows that decreased CD36 expression was posttranscriptional and not directly related to PEs phagocytosis. In addition, these culture models suggest that the reduced capacity of TNF-α production occurred in 2 phases. The early phase (24 hr) appeared to be CD36 dependent and the second phase (48 hr) was due to a soluble factor produced by PEs. These observations suggest that the control of the TNF-α production in malaria by monocytes was not entirely dependent on the phagocytosis of PEs by CD36 and that soluble factors produced by PEs could play a role in this process.
机译：严重的疟疾与宿主防御系统无法控制寄生虫复制，促炎性细胞因子（如肿瘤坏死因子-α（TNF-α））的过度分泌以及在重要生命的微循环中隔离寄生红细胞（PEs）有关器官。清道夫受体CD36，被称为主要螯合受体，也已被确定为介导单核细胞和巨噬细胞介导PE非调理吞噬作用的重要因素。这种吞噬作用的特定结果是寄生虫诱导的TNF-α分泌减少。我们评估了恶性疟原虫感染患者单核细胞中CD36水平和脂多糖（LPS）诱导的TNF-α产生的变化，以及存在PE的体外变化。来自感染患者和体外培养的单核细胞均显示LPS诱导的CD36表达减少和TNF-α产生减少。使用不与单核细胞和PEs接触或在从单核细胞和PEs孵育获得的可溶性上清液存在的情况下进行的孵育测定，这项研究表明CD36表达的降低是转录后的，与PEs的吞噬作用没有直接关系。另外，这些培养模型表明TNF-α产生的能力降低发生在两个阶段。早期阶段（24小时）似乎是CD36依赖性的，而第二阶段（48小时）则是由于PE产生的可溶性因子。这些观察结果表明，单核细胞控制疟疾中的TNF-α的产生并不完全取决于CD36对PE的吞噬作用，并且PE产生的可溶性因子可能在此过程中起作用。

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