Upregulation of miR-155 regulates group 2 innate lymphoid cells by targeting c-maf in allergic rhinitis
| Autor: | Meiqun Wang, Xinhua Zhu, Yaqiong Zhu, Zhi Wang, Yuehui Liu |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Mucous membrane of nose miR-155 Pathogenesis 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine Immune system Th2 Cells Downregulation and upregulation Medicine Animals Humans Antagomir Lymphocytes Pathological Pharmacology Mice Inbred BALB C business.industry Innate lymphoid cell Rhinitis Allergic Seasonal Immunity Innate Up-Regulation MicroRNAs Nasal Mucosa 030104 developmental biology chemistry Proto-Oncogene Proteins c-maf Immunology Cytokines business Protein Processing Post-Translational 030217 neurology & neurosurgery |
| Zdroj: | European journal of pharmacology. 887 |
| ISSN: | 1879-0712 |
| Popis: | Group 2 innate lymphoid cells (ILC2s) and Th2 type immune response are critically involved in the pathogenesis of allergic rhinitis (AR), and this pathological process is influenced by microRNAs-mediated post-transcriptional regulation. The present study investigated the adaptation and function of miR-155 in AR patients and mouse model. We found that significantly increased miR-155 expression (1.63 ± 0.12 vs. 0.92 ± 0.11 in human, and 1.68 ± 0.15 vs. 1.06 ± 0.06 in mice) and ILC2s activity in nasal mucosa and serum in AR patients and mice. Administration of miR-155 antagomir significantly reduced the activity of ILC2s in nasal mucosa, suppressed the production of Th2 cytokines in serum and nasal mucosa, and alleviated the airway inflammation and allergic symptoms in AR mice, while miR-155 agomir increased ILC2s activity and production of Th2 cytokines and induced airway inflammation and allergic symptoms in control mice. Meanwhile, the expression of transcriptional factor c-Maf (0.57 ± 0.05 vs. 0.37 ± 0.04) in nasal mucosa in AR mice, which was significantly recovered by miR-155 antagomir (0.56 ± 0.04). Treatment with miR-155 agomir decreased c-Maf expression in nasal mucosa in control mice. This synchronized with the similar pattern in the current observations that miR-155 regulated Th2 cytokine (IL-4, IL-5, IL-9 and IL-13) production, airway inflammation and allergic symptoms in AR mice. Together, upregulation miR-155 suppressed the expression of transcriptional factor c-Maf and was critically involved in the ILC2s activation, which contributed to the airway inflammation and allergic symptoms in AR. |
| Databáze: | OpenAIRE |
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