Stoiser B, Looareesuwan S, Thalhammer F, Daxböck F, Chullawichit S, El-Menyawi I, Graninger W, Burgmann H
Department of Internal Medicine I, Division of Infectious Diseases, Währinger Gürtel 18-20, A-1090 Vienna, Austria.
Eur Cytokine Netw. 2000 Mar;11(1):75-80.
Involvement of neutrophils in the control of blood parasites in malaria has been reported. Both, mononuclear phagocytes and neutrophils are known to be stimulated by cytokines such as TNF-alpha in order to augment the defence potency against the parasites. Previously, it has been shown that serum-G-CSF concentrations are increased in patients with bacterial sepsis. In vitro studies have shown that P. falciparum - infected erythrocytes induce the release of G-CSF by several cells such as endothelial cells and monocytes, however, nothing is known about G-CSF serum concentrations during the clinical course of severe P. falciparum malaria. Thus, it was the aim of the present study to investigate the time course for G-CSF serum concentrations in patients with complicated P. falciparum malaria, and to correlate these values with other mediators of inflammation and hematopoesis. Twenty-six patients suffering from complicated P. falciparum malaria were included in the study, and 20, age and sex matched, healthy volunteers were used as the negative control group. Serum samples for determination of G-CSF were taken on day 0, 7 and 14, and measured by ELISA. We found significantly increased serum concentrations of G-CSF in patients with complicated P. falciparum malaria on day 0, values decreasing to within the normal range by day 7. A significant correlation was found between G-CSF (d0) and procalcitonin, the parasite count, erythropoietin and macrophage inflammatory protein, however no correlation could be shown for the neutrophil count. In conclusion, on the day of hospital admission, elevated serum concentrations of G-CSF were detected in patients with complicated P. falciparum malaria, which might indicate a role of G-CSF in the acute defence mechanism against the parasites.
已有报道称中性粒细胞参与疟疾中血液寄生虫的控制。已知单核吞噬细胞和中性粒细胞都会受到细胞因子（如肿瘤坏死因子-α）的刺激，以增强对寄生虫的防御能力。此前，研究表明细菌性败血症患者血清中粒细胞集落刺激因子（G-CSF）浓度会升高。体外研究表明，恶性疟原虫感染的红细胞可诱导内皮细胞和单核细胞等多种细胞释放G-CSF，然而，对于严重恶性疟原虫疟疾临床病程中G-CSF血清浓度情况尚不清楚。因此，本研究的目的是调查复杂型恶性疟原虫疟疾患者G-CSF血清浓度的时间变化过程，并将这些值与其他炎症和造血介质相关联。本研究纳入了26例患有复杂型恶性疟原虫疟疾的患者，并将20名年龄和性别匹配的健康志愿者作为阴性对照组。在第0天、第7天和第14天采集用于测定G-CSF的血清样本，并通过酶联免疫吸附测定法（ELISA）进行测量。我们发现，复杂型恶性疟原虫疟疾患者在第0天血清G-CSF浓度显著升高，到第7天时降至正常范围内。G-CSF（第0天）与降钙素原、寄生虫计数、促红细胞生成素和巨噬细胞炎性蛋白之间存在显著相关性，然而与中性粒细胞计数未显示出相关性。总之，在医院入院当天，复杂型恶性疟原虫疟疾患者血清G-CSF浓度升高，这可能表明G-CSF在针对寄生虫感染的急性防御机制中发挥作用。
