MiR-193b-3p Regulates TLR4 Expression to Inhibit Inflammation by Targeting ETS1 in Allergic Rhinitis.

INTRODUCTION: Allergic rhinitis (AR) is identified as a multifactorial disease caused by the interaction of genes and surroundings, which is difficult to cure. MicroRNAs were reported to be engaged in AR development. Here, we aimed to seek the anti-inflammatory effects and regulatory mechanism of miR-193b-3p in AR. METHODS: Mucosal tissues from AR patients and healthy volunteers were collected, and human nasal epithelial cells (HNECs) were treated with IL-13 to establish a cell model of AR. The gene expression of miR-193b-3p, ETS1, TLR4, GM-CSF, eotaxin, and MUC5AC was determined by RT-qPCR. The protein levels of ETS1 and TLR4 were examined using Western blot. Enzyme-linked immunosorbent assay was performed to measure protein concentration of GM-CSF, eotaxin, and MUC5AC in cell supernatant. Dual luciferase assay was applied to verify the interaction among miR-193b-3p, ETS1, and TLR4. RESULTS: The expression of miR-193b-3p was declined in clinical samples from AR patients and in IL-13-induced HNECs, while the mRNA and protein levels of ETS1 and TLR4 were elevated. MiR-193b-3p overexpression or ETS1 silencing notably decreased the mRNA and protein levels of GM-CSF, eotaxin, and MUC5AC in IL-13-treated HNECs. Mechanistically, miR-193b-3p directly combined with ETS1 to silence ETS1 expression. ETS1 promoted the transcriptional activity of TLR4 through interacting with TLR4 promoter. Furthermore, rescue experiments revealed that ETS1 overexpression abolished miR-193b-3p sufficiency-mediated suppression of the mRNA and protein levels of GM-CSF, eotaxin, and MUC5AC in IL-13-treated HNECs. Similarly, TLR4 overexpression compromised the inhibitory impacts of ETS1 downregulation on the mRNA and protein levels of GM-CSF, eotaxin, and MUC5AC in IL-13-induced HNECs. DISCUSSION: MiR-193b-3p repressed IL-13-induced inflammatory response in HNECs by suppressing ETS1/TLR4 axis, which indicated that miR-193b-3p might be a therapeutic target for AR treatment.

[Behavior research of allergic rhinitis with adenoid hypertrophy in children].

OBJECTIVE: To investigate the behavior difference of allergic rhinitis with adenoid hypertrophy between study group and control group. METHOD: One hundred and seventeen children diagnosed as allergic rhinitis with adenoid hypertrophy were enrolled in our study were divided into study group and control group. Forty-two children treated with local steroid nasal spray for two to three months and antihistamine were control group. Seventy-five children treated with endoscopic adenoidectomy and drug treatment were study group; All children' parents were inquired for their clinical presentation. RESULT: No distinctive differences were found between the two groups (P > 0.05) in adenoid hypertrophy, accompanying nasal problems and clinical questionnaire scoring. Significant statistical distinction were found (P < 0.05) in snoring, sleep disturbance and frequent arousal, nasal obstructive moth-breathing, and recurrent respiratory tract infection between the two groups after three-month follow up. CONCLUSION: Endoscopic adenoidectomy should be taken into account for allergic rhinitis with adenoid hypertrophy in children. Adenoidectomy would be useful for the improvement of behavior symptoms.