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

Abstract

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, apoptosis associated speck like protein containing a card, cleaved caspase-1 and il-1β 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.

Phosphatidylethanolamine-binding protein 1 (PEBP1) mediates the regulatory role of microRNAs (miRNAs)-205-5p in degranulation and histamine release

“…The results in our experiments suggested that increased miR-205-5P expression altered the levels of Th1/Th2 cytokines in OVA-induced AR, thereby affecting IgE production. Furthermore, it was reported that miR‑205‑5p knockdown improved AR by targeting BCL6 [ 12 ]. Based on the present study, miR‑205‑5p bound to 3UTR of PEBP1 and regulated its expression to involve in the pathogenesis of AR.…”

“…Current studies have noted that miRNA is associated with a variety of clinical diseases, including AR, chronic sinusitis, asthma, atopic dermatitis and other immune diseases [ 8–11 ]. A recent report demonstrated that miR‑205‑5p was involved in inflammatory response in AR with the help of B‑cell lymphoma 6 [ 12 ]. Previous research has found that PEBP1, also called RAF1 kinase inhibitory protein (RKIP1), can increase allergic responses in mast cells [ 13 ], indicating that PEBP1 was involved in AR.…”

Comprehensive bioinformatics method to explore immune-related genes in the pathogenesis of myocardial infarction

“…Chen D found that BCL6 may have a negative regulatory effect on NLRP3 (nucleotide-binding oligomerization domain-like receptor family pyrin domain 3) by binding to it and attenuating inflammation in human renal tubular epithelial cells and in vivo [30] . Zhang S found that BCL6 can act as a target of mir-205-5p and mir-205-5p knockdown can reduce the inflammatory response in allergic rhinitis by targeting BCL6 [31] . Jager A found that Bcl6 has an important regulatory function in macrophages, limiting TLR-induced inflammatory responses [32] .…”

XBP1 Regulates the Transcription of HIF-1a in BALB/c Mice with Chronic Rhinosinusitis without Polyps

“…After the operation, the mice were bred normally for 90 d. After 90 d, the mice were euthanized through 150 mg/kg pentobarbital sodium and diagnosed as CRSsNP by pathological examination, and the nasal mucosal tissues were subsequently collected [ 12 ]. For lentivirus treatment, on the basis of the CRSsNP modeling, we administered 20 μ L lentiviruses to the mice intranasally on the 2 nd d after the operation [ 13 ], followed by the same steps as for the CRSsNP model establishment.…”