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Mast cells (MCs) are the major effector cells of allergic rhinitis (AR). The present study aimed to investigate the effects of C-C chemokine receptor type 3 (CCR3) on the proliferation, apoptosis, chemotaxis and activated degranulation of mouse MCs. Mouse bone marrow-derived MCs were cultured in vitro, purified and identified using toluidine blue staining and flow cytometry. Three different CCR3-short hairpin (shRNA) lentiviral vectors were constructed and transfected into MCs, and the mRNA and protein expression levels of CCR3 were assessed by reverse transcription-quantitative PCR and western blotting. Proliferation and apoptosis of the MCs were measured using Cell Counting kit-8 (CCK-8) assays and flow cytometry, respectively. MC chemotaxis was assessed by Transwell assay and quantified using flow cytometry. The activation of MC degranulation was examined using ELISAs. The results demonstrated that MCs were appropriately isolated, and identified that CCR3-shRNA2 presented the higher knockdown effect among the three shRNAs tested. Following 96 h of transfection, the results of CCK-8 and flow cytometry assays demonstrated that CCR3-shRNA2 inhibited MC proliferation and promoted MC apoptosis. The results from the Transwell assay indicated that CCR3-shRNA2 restrained MC chemotaxis, whereas ELISA results demonstrated that CCR3-shRNA2 suppressed MC degranulation. In conclusion, CCR3-shRNA2 effectively downregulated CCR3 mRNA and protein expression levels in mouse MCs. In addition, CCR3-shRNA2 promoted MC apoptosis and suppressed the proliferation, chemotaxis and degranulation of mouse MCs, suggesting that CCR3-shRNA2 may serve as a therapeutic tool for the treatment of allergic rhinitis. [ABSTRACT FROM AUTHOR]

The present study aimed to explore the microRNA‑let‑7e (miR‑let‑7e) expression in allergic rhinitis (AR), and to investigate the underlying molecular mechanisms. miR‑let‑7e expression in the nasal mucosa of mice and patients with AR were detected. The expression levels of three inflammatory factors, including histamine, immunoglobulin E and tumor necrosis factor‑α (TNF‑α), in the blood of AR mice and in interleukin (IL)‑13‑stimulated nasal epithelial cells (NECs) were also measured. Furthermore, the target gene of miR‑let‑7e was predicted and validated using a luciferase reporter assay. The expression levels of Janus kinase 1 (JAK1) and signal transducer and activator of transcription 3 (STAT3) were detected. The results demonstrated that miR‑let‑7e was downregulated in patients and mice with AR compared with the controls. In addition, the expression levels of inflammatory factors were higher in the blood of mice with AR compared with the control group, while miR‑let‑7e overexpression inhibited these levels in AR mice and IL‑13‑stimulated NECs. Furthermore, suppressor of cytokine signaling 4 (SOCS4) was revealed as a potential target gene of miR‑let‑7e and was negatively regulated by miR‑let‑7e. Overexpression of SOCS4 abrogated the anti‑inflammatory activity of miR‑let‑7e overexpression. Finally, miR‑let‑7e overexpression activated the JAK1/STAT3 signaling pathway. In conclusion, miR‑let‑7e may serve an important role in the progression and development of AR, while overexpression of miR‑let‑7e had an anti‑inflammatory effect by targeting SOCS4, which may be achieved by activation of the JAK1/STAT3 signaling pathway. [ABSTRACT FROM AUTHOR]