Canine leishmaniasis (CanL) is caused by the intracellular parasite Leishmania infantum. Prostaglandin E2 (PGE2 ) exerts potent regulatory effects on the immune system in experimental model Leishmania infection, but this influence has not yet been studied in CanL. In this study, PGE2 and PGE2 receptor levels and the regulatory effect of PGE2 on arginase activity, NO2 , IL-10, IL-17, IFN-γ, TNF-α and parasite load were evaluated in cultures of splenic leucocytes obtained from dogs with CanL in the presence of agonists and inhibitors. Our results showed that splenic leucocytes from dogs with CanL had lower EP2 receptor levels than those of splenic leucocytes from healthy animals. We observed that NO2 levels decreased when the cells were treated with a PGE2 receptor agonist (EP1/EP2/EP3) or COX-2 inhibitor (NS-398) and that TNF-α, IL-17 and IFN-γ cytokine levels decreased when the cells were treated with a PGE2 receptor agonist (EP2) or PGE2 itself. The parasite load in splenic leucocyte cell cultures from dogs with CanL decreased after stimulation of the cells with PGE2 . We conclude that Leishmania infection of dogs modulates PGE2 receptors and speculate that the binding of PGE2 to its receptors may activate the microbicidal capacity of cells.

中文翻译：

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PGE 2对犬利什曼病的杀菌活性和炎性细胞因子的调节作用。

犬利什曼病（CanL）是由胞内寄生虫婴儿利什曼原虫引起的。前列腺素E2（PGE2）在实验模型利什曼原虫感染中对免疫系统产生有效的调节作用，但尚未在CanL中研究这种影响。在这项研究中，PGE2和PGE2受体水平以及PGE2对精氨酸酶活性，NO2，IL-10，IL-17，IFN-γ，TNF-α和寄生虫负荷的调节作用在从狗获得的脾白细胞培养物中进行了评估。激动剂和抑制剂存在下的CanL。我们的结果表明，患有CanL的狗的脾白细胞的EP2受体水平低于健康动物的脾白细胞。我们观察到，当用PGE2受体激动剂（EP1 / EP2 / EP3）或COX-2抑制剂（NS-398）处理细胞时，NO2含量降低，而TNF-α，当用PGE2受体激动剂（EP2）或PGE2本身处理细胞时，IL-17和IFN-γ细胞因子水平降低。用PGE2刺激的CanL犬脾脏白细胞培养中的寄生虫负荷降低。我们得出的结论是，狗的利什曼原虫感染会调节PGE2受体，并推测PGE2与其受体的结合可能会激活细胞的杀菌能力。