Knockdown of miR-205-5p alleviates the inflammatory response in allergic rhinitis by targeting B-cell lymphoma 6

Allergic rhinitis (AR) is an IgE-mediated upper airway disease with a high worldwide prevalence. MicroRNA (miR)-205-5p upregulation has been observed in AR; however, its role is poorly understood. The aim of the present study was to investigate the effect of miR-205-5p on AR-associated inflammation. To establish an AR model, BALB/c mice were sensitized using an intraperitoneal injection of ovalbumin (OVA) on days 0, 7 and 14, followed by intranasal challenge with OVA on days 21-27. A lentiviral sponge for miR-205-5p was used to downregulate miR-205-5p in vivo via intranasal administration on days 20-26. Reverse transcription-quantitative PCR revealed that miR-205-5p was upregulated in AR mice. Notably, miR-205-5p knockdown reduced the frequency of nose-rubbing and sneezing, and attenuated pathological alterations in the nasal mucosa. The levels of total and OVA-specific IgE, cytokines IL-4, IL-5 and IL-13, and inflammatory cells, were decreased by miR-205-5p knockdown in AR mice. In addition, miR-205-5p knockdown inhibited nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation by reducing the expression levels of NLRP3, apoptosisassociated specklike protein containing a CARD, cleaved caspase-1 and IL-1 beta by western blot analysis. B-cell lymphoma 6 (BCL6) was confirmed as a target of miR-205-5p by luciferase reporter assay. In conclusion, the present findings suggested that miR-205-5p knockdown may attenuate the inflammatory response in AR by targeting BCL6, which may be a potential therapeutic target for AR.