tgf-β targeted by mir-27a modulates anti-parasite responses of immune system

Background: immune cells and their secreted cytokines are known as the first barrier against pathogens. leishmania major as an intracellular protozoan produces anti-inflammatory cytokines that lead to proliferation and survival of the parasite in the macrophages. mirnas are small non-coding rna molecules that regulate mrnas expression. we aimed to investigate the relationship between the expression of tgf-β and a bioinformatically candidate mirna, in leishmaniasis as a model of tgf-β overexpression.methods: the mirnas that target tgf-β -3´utr were predicted and scored by bioinformatic tools. after cloning of tgf-β-3'utr in psi-check tm- 2 vector, targeting validation was confirmed using luciferase assay. after mirna mimic transfection, the expression of mir-27a, tgf-β, as well as nitric oxide concentration was evaluated.results: mir-27a received the highest score for targeting tgf-β in bioinformatic predictions. luciferase assay confirmed that mir-27a is targeting tgf-β-3'utr, since mir-27a transfection decreased the luciferase activity. after mirna transfection, tgf-β expression and nitric oxide concentration were declined in l. major infected macrophages.conclusion: bioinformatic prediction, luciferase assay, and mirna transfection results showed that mir-27a targets tgf-β. since mirna and cytokine-base therapies are developing in infectious diseases, finding and validating mirnas targeting regulatory cytokines can be a novel strategy for controlling and treating leishmaniasis.