Lamikanra Abigail A, Brown Douglas, Potocnik Alexandre, Casals-Pascual Climent, Langhorne Jean, Roberts David J
Nuffield Department of Clinical Laboratory Sciences and National Blood Service Oxford Centre, John Radcliffe Hospital, Oxford, United Kingdom.
Blood. 2007 Jul 1;110(1):18-28. doi: 10.1182/blood-2006-09-018069. Epub 2007 Mar 6.
Severe malaria is manifest by a variety of clinical syndromes dependent on properties of both the host and the parasite. In young infants, severe malarial anemia (SMA) is the most common syndrome of severe disease and contributes substantially to the considerable mortality and morbidity from malaria. There is now growing evidence, from both human and mouse studies of malaria, to show that anemia is due not only to increased hemolysis of infected and clearance of uninfected red blood cells (RBCs) but also to an inability of the infected host to produce an adequate erythroid response. In this review, we will summarize the recent clinical and experimental studies of malaria to highlight similarities and differences in human and mouse pathology that result in anemia and so inform the use of mouse models in the study of severe malarial anemia in humans.
重症疟疾表现为多种临床综合征,这取决于宿主和寄生虫的特性。在幼儿中,重症疟疾贫血(SMA)是最常见的重症疾病综合征,也是疟疾导致高死亡率和高发病率的主要原因。目前,来自人类和小鼠疟疾研究的证据越来越多,表明贫血不仅是由于受感染红细胞的溶血增加和未感染红细胞(RBC)的清除,还由于受感染宿主无法产生足够的红系反应。在这篇综述中,我们将总结近期疟疾的临床和实验研究,以突出人类和小鼠病理学中导致贫血的异同,从而为小鼠模型在人类重症疟疾贫血研究中的应用提供参考。