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疟疾相关性急性呼吸窘迫综合征的发病机制。

Pathogenesis of malaria-associated acute respiratory distress syndrome.

机构信息

Laboratory of Immunobiology, Rega Institute for Medical Research, KU Leuven-University of Leuven, Minderbroedersstraat 10, 3000 Leuven, Belgium.

出版信息

Trends Parasitol. 2013 Jul;29(7):346-58. doi: 10.1016/j.pt.2013.04.006. Epub 2013 Jun 3.

Abstract

Malaria-associated acute respiratory distress syndrome (MA-ARDS) is an increasingly reported, often lethal, and incompletely understood complication of malaria. We discuss and compare the pathogenesis of MA-ARDS in patients and in different murine models, including recent models without cerebral involvement, and summarize the roles of different leukocyte subclasses, adhesion molecules, cytokines, and chemokines. In patients as well as in mice, severe edema and impaired gas exchange are associated with abundant inflammatory infiltrates consisting of mainly mononuclear cells and parasite sequestration, and the pathogenesis appears different from cerebral malaria (CM). Experimental anti-inflammatory interventions are successful in mice and remain to be validated in patients.

摘要

疟疾相关性急性呼吸窘迫综合征(MA-ARDS)是一种日益被报道的、常常致命的且尚未完全被理解的疟疾并发症。我们讨论并比较了 MA-ARDS 在患者和不同的小鼠模型中的发病机制,包括最近没有脑受累的模型,并总结了不同白细胞亚群、黏附分子、细胞因子和趋化因子的作用。在患者和小鼠中,严重的水肿和气体交换受损与主要由单核细胞和寄生虫隔离组成的丰富炎症浸润有关,其发病机制与脑型疟疾(CM)不同。实验性抗炎干预在小鼠中是成功的,仍有待在患者中验证。

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