MicroRNAs (miRNAs) are non-coding and regulate
broad biological processes including immune responses. MiRNAs fine-tune gene
expression post-transcriptionally by inhibiting translation or inducing
degradation of target mRNAs. Their contributions to the function of specific
immune cells still remain largely unknown. MiR-487b was initially discovered in
human neuroblastoma and it plays critical role in cell growth, however its
function in immunity remain unclear. In this study, we report that miR-487b can
suppress both mRNA and protein levels of IL-33 during the differentiation of
bone-marrow derived macrophages (BMDM), thus suppressing IL-33-enhanced expression
of antigen presenting and co-stimulatory molecules and inflammatory mediators. Luciferase
assay showed that miR-487b could bind to the IL-33 untranslated region. We also
confirmed that IL-33 promotes the activation of BMDM by increasing the
expression of MHC -I and –II, CD80, CD86 and inducible nitric oxide synthase (iNOS)
in a dose-dependent manner. LPS, a typical TLR4 ligand, decreases miR-487b
expression, increases IL-33 expression and promotes BMDM activation. Inhibition
of miR-487b resulted in the elevated IL-33 expression, thus augmenting the
expression of inflammatory factors of LPS-stimulated BMDM. Therefore, miR-487b
plays an important role in the regulation of homeostasis and the activation of
macrophages by targeting IL-33 transcripts. Our results provide an important
link for triggering macrophage’s inflammatory response.