Concomitant experimental co-infection by Plasmodium berghei NK65 and Ascaris suum downregulates immunological responses and impairs lung function

Ascariasis and malaria are highly prevalent parasitic diseases in tropical regions and often overlap in endemic areas, contributing to high morbidity and mortality rates in areas with poor sanitary conditions. Several studies aiming to correlate the effects of Ascaris-Plasmodium coinfections have contradictory and inconclusive results. In this context, we investigated parasitological and immunopathological aspects of the lung in an experimental concomitant coinfection by Plasmodium berghei NK65-NY and Ascaris suum during larval ascariasis. The most important findings of P. berghei NK65-NY and A. suum coinfection results in Plasmodium-driven downregulation of the lung immune response that leads to an increase in larval migration in the lungs, as evidenced by the decrease in larvae recovered in the lung parenchyma and the increase in larvae recovered in the airways. This scenario is implicated in an intense hemorrhage in the airways and, consequently, in the commitment of respiratory function that results in high morbidity and early mortality. Taken together, our results suggest that this coinfection may potentiate Ascaris-associated pathology by the downmodulation of the Ascaris-specific immune response, resulting in the early death of affected animals.<br>蛔虫病与疟疾均为热带地区高流行寄生虫病，且二者常于流行区域共存，在卫生条件恶劣的地区可引发极高的发病率与死亡率。既往多项旨在探究蛔虫（Ascaris）与疟原虫（Plasmodium）共感染效应的研究，所得结论相互矛盾且尚无定论。鉴于此，本研究针对幼虫移行期蛔虫感染状态下，伯氏疟原虫（Plasmodium berghei）NK65-NY株与猪蛔虫（Ascaris suum）实验性共感染的肺部寄生虫学与免疫病理学特征展开探究。本研究最核心的发现为：伯氏疟原虫介导的肺部免疫应答下调，可增强肺部幼虫移行能力，该结论可通过肺实质中检出的幼虫数量减少、而气道内检出的幼虫数量增加得到验证。此种共感染状态可引发气道严重出血，进而损害呼吸功能，最终导致高发病率与早期死亡。综合来看，本研究结果表明，此种共感染可通过下调蛔虫特异性免疫应答，加重蛔虫相关病理损伤，最终导致感染动物早期死亡。