Laboratory of Immunology and Genomics of Parasites, Institute of Biological Sciences, Department of Parasitology, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Laboratory of Protozooses, Institute of Biological Sciences, Department of General Pathology, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Malar J. 2021 Jul 1;20(1):296. doi: 10.1186/s12936-021-03824-w.
Ascariasis and malaria are highly prevalent parasitic diseases in tropical regions and often have overlapping endemic areas, contributing to high morbidity and mortality rates in areas with poor sanitary conditions. Several studies have previously aimed to correlate the effects of Ascaris-Plasmodium coinfections but have obtained contradictory and inconclusive results. Therefore, the present study aimed to investigate parasitological and immunopathological aspects of the lung during murine experimental concomitant coinfection by Plasmodium berghei and Ascaris suum during larvae ascariasis.
C57BL/6J mice were inoculated with 1 × 10 P. berghei strain NK65-NY-infected red blood cells (iRBCs) intraperitoneally and/or 2500 embryonated eggs of A. suum by oral gavage. P. berghei parasitaemia, morbidity and the survival rate were assessed. On the seventh day postinfection (dpi), A. suum lung burden analysis; bronchoalveolar lavage (BAL); histopathology; NAG, MPO and EPO activity measurements; haematological analysis; and respiratory mechanics analysis were performed. The concentrations of interleukin (IL)-1β, IL-12/IL-23p40, IL-6, IL-4, IL-33, IL-13, IL-5, IL-10, IL-17A, IFN-γ, TNF and TGF-β were assayed by sandwich ELISA.
Animals coinfected with P. berghei and A. suum show decreased production of type 1, 2, and 17 and regulatory cytokines; low leukocyte recruitment in the tissue; increased cellularity in the circulation; and low levels of NAG, MPO and EPO activity that lead to an increase in larvae migration, as shown by the decrease in larvae recovered in the lung parenchyma and increase in larvae recovered in the airway. This situation leads to severe airway haemorrhage and, consequently, an impairment respiratory function that leads to high morbidity and early mortality.
This study demonstrates that the Ascaris-Plasmodium interaction is harmful to the host and suggests that this coinfection may potentiate Ascaris-associated pathology by dampening the Ascaris-specific immune response, resulting in the early death of affected animals.
在热带地区，蛔虫病和疟疾是高度流行的寄生虫病，往往有重叠的流行地区，在卫生条件差的地区导致高发病率和死亡率。以前有几项研究旨在探讨蛔虫-疟原虫混合感染的影响，但得到的结果相互矛盾，没有定论。因此，本研究旨在探讨伯氏疟原虫和猪蛔虫幼虫期蛔虫病时小鼠实验性同时感染对肺的寄生虫学和免疫病理学的影响。
C57BL/6J 小鼠经腹腔接种 1×10 个伯氏疟原虫 NK65-NY 感染的红细胞（iRBC）和/或经口服灌胃 2500 个猪蛔虫卵。评估伯氏疟原虫的寄生虫血症、发病率和存活率。在感染后第 7 天（dpi），进行猪蛔虫肺负荷分析；支气管肺泡灌洗（BAL）；组织病理学；NAG、MPO 和 EPO 活性测量；血液学分析；和呼吸力学分析。通过夹心 ELISA 测定白细胞介素（IL）-1β、IL-12/IL-23p40、IL-6、IL-4、IL-33、IL-13、IL-5、IL-10、IL-17A、IFN-γ、TNF 和 TGF-β 的浓度。
同时感染伯氏疟原虫和猪蛔虫的动物表现出 1 型、2 型和 17 型以及调节性细胞因子产生减少；组织中白细胞募集减少；循环中细胞增多；NAG、MPO 和 EPO 活性水平降低，导致幼虫迁移增加，表现为肺实质中回收的幼虫减少，气道中回收的幼虫增加。这种情况导致严重的气道出血，进而导致呼吸功能受损，导致高发病率和早期死亡率。
本研究表明，蛔虫-疟原虫相互作用对宿主有害，并表明这种混合感染可能通过抑制蛔虫特异性免疫反应，加剧与蛔虫相关的病理，导致受感染动物的早期死亡。
