miR-155 is upregulated in patients with active tuberculosis and inhibits apoptosis of monocytes by targeting FOXO3

The aim of the present study was to investigate the association between microRNA (miR)-155 and apoptosis of monocytes infected by Mycobacterium tuberculosis, to examine the effect of forkhead box O3 (FOXO3) on miR-155. The present study analysed the apoptosis of CD14(+) in the peripheral blood of patients with active tuberculosis, disposed the THP-1 human monocytic cell line by BCG and examined the expression of miR-155. Furthermore, the expression of FOXO3 in THP-1 cells was determined, and wild- and mutant-type luciferase reporter plasmids containing FOXO3 3'-untranslated regions (UTRs) were constructed to analyse the expression of luciferase. Finally, an over-expression plasmid was constructed, and THP-1 cells were transfected with control miRNA, miR-155 and the plasmid, which revealed that miR-155 inhibited the apoptosis of THP-1 cells. miR-155 in the THP-1 cells infected by BCG was upregulated and apoptosis also increased. However, the apoptosis declined when the cells were transfected with the control miRNA and miR-155. Folllowing transfection with miR-155, the expression of FOXO3 decreased. Transfection with miR-155 and the FOXO3 3'-UTRs significantly reduced luciferase, and overexpression of FOXO3 reversed the inhibitory role of miR-155. From these results, it was concluded that mycobacteria can improve the level of miR-155, while BCG can induce apoptosis in THP-1 cells. The results suggested FOXO3 is a downstream target gene of miR-155, which combines 3'-UTRs to inhibit the expression of FOXO3.