Laboratório de Imunofarmacologia, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz, Rio de Janeiro, RJ, Brazil.
Universidade Iguaçu, Nova Iguaçu, RJ, Brazil.
Malar J. 2020 Jul 1;19(1):234. doi: 10.1186/s12936-020-03305-6.
Malaria-triggered lung injury can occur in both severe and non-severe cases. Platelets may interact with parasitized erythrocytes, leukocytes and endothelium. These interactions can lead to microvessel obstructions and induce release of inflammatory mediators. Induction of the haem oxygenase enzyme is important in the host's response to free haem and to several other molecules generated by infectious or non-infectious diseases. In addition, an important role for the haem oxygenase-1 isotype has been demonstrated in experimental cerebral malaria and in clinical cases. Therefore, the present work aims to determine the influence of haem oxygenase in thrombocytopaenia and acute pulmonary injury during infection with Plasmodium berghei strain NK65.
C57BL/6 mice were infected with P. berghei and analysed 7-10 days post-infection. For each experiment, Cobalt Protoporphyrin IX/CoPPIX or saline were administered. Bronchoalveolar lavage fluid was used for total and differential leukocyte count and for protein measurement. Lungs were used for histological analyses or for analysis of cytokines and western blotting. The lung permeability was analysed by Evans blue dye concentration. Platelet-leukocyte aggregate formation was assayed using the flow cytometer.
Plasmodium berghei NK65 infection generated an intense lung injury, with increased levels of inflammatory mediators, oedema, and cell migration into the lung. Plasmodium berghei infection was also accompanied by marked thrombocytopaenia and formation of platelet-leukocyte aggregates in peripheral blood. Treatment with the HO-1 inducer cobalt protoporphyrin IX (CoPPIX) modified the inflammatory response but did not affect the evolution of parasitaemia. Animals treated with CoPPIX showed an improvement in lung injury, with decreased inflammatory infiltrate in the lung parenchyma, oedema and reduced thrombocytopaenia.
Data here presented suggest that treatment with CoPPIX inducer leads to less severe pulmonary lung injury and thrombocytopaenia during malaria infection, thus increasing animal survival.
疟疾引起的肺损伤可发生在严重和非严重病例中。血小板可能与寄生的红细胞、白细胞和内皮细胞相互作用。这些相互作用可导致微血管阻塞,并诱导炎症介质释放。血红素加氧酶的诱导在宿主对游离血红素和由感染或非感染性疾病产生的几种其他分子的反应中很重要。此外,血红素加氧酶-1 同工型在实验性脑疟疾和临床病例中发挥了重要作用。因此,本工作旨在确定血红素加氧酶在感染 Plasmodium berghei 株 NK65 时血小板减少症和急性肺损伤中的影响。
C57BL/6 小鼠感染 P. berghei 并在感染后 7-10 天进行分析。对于每个实验,给予钴原卟啉 IX/CoPPIX 或生理盐水。用支气管肺泡灌洗液进行总白细胞和分类白细胞计数以及蛋白测量。用肺进行组织学分析或细胞因子分析和蛋白质印迹分析。通过 Evans 蓝染料浓度分析肺通透性。使用流式细胞仪检测血小板-白细胞聚集体的形成。
Plasmodium berghei NK65 感染导致强烈的肺损伤,炎症介质水平升高、水肿和细胞向肺内迁移。Plasmodium berghei 感染还伴有明显的血小板减少症和外周血中血小板-白细胞聚集体的形成。血红素加氧酶-1 诱导剂钴原卟啉 IX(CoPPIX)的治疗改变了炎症反应,但不影响寄生虫血症的演变。用 CoPPIX 治疗的动物显示肺损伤改善,肺实质中的炎症浸润减少,水肿减轻,血小板减少症减轻。
本文提供的数据表明,用 CoPPIX 诱导剂治疗可导致疟疾感染期间肺损伤和血小板减少症减轻,从而提高动物的存活率。