MicroRNA-155 plays critical effects on Th2 factors expression and allergic inflammatory response in type-2 innate lymphoid cells in allergic rhinitis

摘要

OBJECTIVE: Allergic rhinitis (AR) is a chronic inflammatory disease. This study aimed to investigate the role of microRNA-155 (miR-155) in type-2 innate lymphoid cells (ILC2s) on AR. PATIENTS AND METHODS: Nasal mucosa tissues and peripheral blood samples were collected. mRNA expression of miR-155, interleukin-25 (IL-25), and interleukin-33 (IL-33) in nasal mucosa tissues was determined using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The AR model was established by injecting with murine IL-33. The frequency of ILC2s was quantified using flow cytometry. MiR-155 agomir or antagomir was intranasally administrated to mice. MiR-155 and helper T cell 2 (Th2) cytokines were measured with quantitative Real-time PCR (qRT-PCR), enzyme-linked immunosorbent assay (ELISA) or Western blotting, respectively. Hematoxylin and eosin (HE) staining was used for the histopathological examination. RESULTS: Compared with controls, mRNA levels miR-155 (p0.001), IL-25 (p0.05), and IL-33 (p0.001) were increased in nasal mucosa tissues of AR patients and AR mice, and ILC2s ratios were enhanced in human peripheral blood (p0.0001), which were much higher after intranasal administration with miR-155 agomir (p0.0001). MiR-155 expression of AR mice was significantly reduced after intranasal administration with miR-155 antagomir (p0.05). Frequencies of ILC2s in human peripheral blood significantly correlated with miR-155 (r=0.4803, p=0.0130). MiR-155 up-regulation markedly increased frequencies of nasal rubbing/sneezing and levels of IL-4, IL-5, IL-9, and IL-13. Pathological changes were worsened after miR-155 agomir and ameliorated after miR-155 antagomir administration. MiR-155 agomir mice (p0.001) showed higher ILC2s, whereas lower in miR-155 antagomir mice compared to AR mice (p0.05). CONCLUSIONS: MiR-155 played critical effects on Th2 factor expression and allergic inflammatory response in ILC2 cells in AR.