School of Pharmacy, Sungkyunkwan University, Suwon 16419, Republic of Korea.
DNBio Pharm. Inc., Research Center, Sungkyunkwan University, Suwon 16419, Republic of Korea.
J Microbiol Biotechnol. 2022 Jun 28;32(6):709-717. doi: 10.4014/jmb.2203.03006. Epub 2022 Apr 18.
Allergic rhinitis (AR), one of the most common inflammatory diseases, is caused by immunoglobulin E (IgE)-mediated reactions against inhaled allergens. AR involves mucosal inflammation driven by type 2 helper T (Th2) cells. Previously, it was shown that the mutant (Δ) could prevent and treat allergic asthma by reducing Th2 responses. However, the underlying mechanism of Δ immunization in AR remains undetermined. Here, we investigated the role of Δ immunization in the development and progression of AR and elucidated potential mechanisms. In an ovalbumin (OVA)-induced AR mice model, Δ alleviated allergic symptoms (frequency of sneezing and rubbing) and reduced TLR2 and TLR4 expression, Th2 cytokines, and eosinophil infiltration in the nasal mucosa. Mechanistically, Δ reduced the activation of the NLRP3 inflammasome in the nasal mucosa by down-regulating the Toll-like receptor signaling pathway. In conclusion, Δ seems to alleviate TLR signaling and NLRP3 inflammasome activation to subsequently prevent AR.
变应性鼻炎(AR)是最常见的炎症性疾病之一,由针对吸入性过敏原的免疫球蛋白 E(IgE)介导的反应引起。AR 涉及由 2 型辅助 T(Th2)细胞驱动的黏膜炎症。先前已经表明,突变体(Δ)可以通过减少 Th2 反应来预防和治疗过敏性哮喘。然而,Δ 免疫接种在 AR 中的潜在机制仍未确定。在这里,我们研究了 Δ 免疫接种在 AR 发展和进展中的作用,并阐明了潜在的机制。在卵清蛋白(OVA)诱导的 AR 小鼠模型中,Δ 减轻了过敏症状(打喷嚏和擦鼻的频率),并降低了 TLR2 和 TLR4 的表达、Th2 细胞因子和嗜酸性粒细胞在鼻黏膜中的浸润。从机制上讲,Δ 通过下调 Toll 样受体信号通路来减少鼻黏膜中 NLRP3 炎性小体的激活。总之,Δ 似乎通过减轻 TLR 信号和 NLRP3 炎性小体的激活来预防 AR。