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 (p<0.001), IL-25 (p<0.05), and IL-33 (p<0.001) were increased in nasal mucosa tissues of AR patients and AR mice, and ILC2s ratios were enhanced in human peripheral blood (p<0.0001), which were much higher after intranasal administration with miR-155 agomir (p<0.0001). MiR-155 expression of AR mice was significantly reduced after intranasal administration with miR-155 antagomir (p<0.05). 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 (p<0.001) showed higher ILC2s, whereas lower in miR-155 antagomir mice compared to AR mice (p<0.05).
Conclusions: MiR-155 played critical effects on Th2 factor expression and allergic inflammatory response in ILC2 cells in AR.