Visceral Leishmaniasis (VL) is a neglected tropical disease, caused by L. infantum in the New World, where dogs are the main reservoir. These parasites can regulate host immune response through miRNA differential expression in the early stages of infection; however such early response has not yet been investigated in the canine model. PBMC from healthy dogs were exposed to L. infantum in vitro and microarray analysis showed an upregulation of miR-206, miR-302d, miR-433, miR-214, miR-493, miR-514, miR-1835, miR-210, miR-539, miR-432, miR-188, miR-345 and downregulation of miR-489 and miR-503 in comparison to non-exposed control cells, at 24 h post-exposure. In silico target prediction showed that the upregulated miRNAs target 1541 genes, which can modulate important pathways involved in the early immune responses, like the “MAPK signaling pathway”, one of the most relevant pathways to Leishmania survival inside host cells. These findings shed light on parasite modulation of host immunity following Leishmania infection, which in turn can be explored for drug development.

内脏利什曼病（VL）是一种被忽视的热带病，由新世界的婴儿乳杆菌引起，那里的狗是主要的水库。这些寄生虫可以在感染的早期通过miRNA差异表达来调节宿主的免疫反应。但是，这种早期反应尚未在犬模型中进行研究。健康犬的PBMC在体外暴露于婴儿乳杆菌，微阵列分析显示miR-206，miR-302d，miR-433，miR-214，miR-493，miR-514，miR-1835，miR-210上调暴露后24小时，与未暴露的对照细胞相比，miR-539，miR-432，miR-188，miR-345，miR-345和miR-489的下调。电脑靶标预测显示，上调的miRNA靶向1541个基因，这些基因可以调节参与早期免疫反应的重要途径，例如“ MAPK信号传导途径”，这是与宿主细胞内利什曼原虫存活最相关的途径之一。这些发现揭示了利什曼原虫感染后宿主免疫的寄生虫调节，进而可用于药物开发。