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Gong, Guoqing, Huang, Peng, Yang, Changliang, Huang, Chengcheng, Zhang, Zhao, Chen, Ruiyao, Sun, Tingfeng, Yang, Guang. (1402). Effects of Blocking NLRP3 Inflammasome on Type II Innate Lymphoid Cell Response in Allergic Rhinitis. سامانه مدیریت نشریات علمی, 20(3), 287-302. doi: 10.22034/iji.2023.96966.2473
Guoqing Gong; Peng Huang; Changliang Yang; Chengcheng Huang; Zhao Zhang; Ruiyao Chen; Tingfeng Sun; Guang Yang. "Effects of Blocking NLRP3 Inflammasome on Type II Innate Lymphoid Cell Response in Allergic Rhinitis". سامانه مدیریت نشریات علمی, 20, 3, 1402, 287-302. doi: 10.22034/iji.2023.96966.2473
Gong, Guoqing, Huang, Peng, Yang, Changliang, Huang, Chengcheng, Zhang, Zhao, Chen, Ruiyao, Sun, Tingfeng, Yang, Guang. (1402). 'Effects of Blocking NLRP3 Inflammasome on Type II Innate Lymphoid Cell Response in Allergic Rhinitis', سامانه مدیریت نشریات علمی, 20(3), pp. 287-302. doi: 10.22034/iji.2023.96966.2473
Gong, Guoqing, Huang, Peng, Yang, Changliang, Huang, Chengcheng, Zhang, Zhao, Chen, Ruiyao, Sun, Tingfeng, Yang, Guang. Effects of Blocking NLRP3 Inflammasome on Type II Innate Lymphoid Cell Response in Allergic Rhinitis. سامانه مدیریت نشریات علمی, 1402; 20(3): 287-302. doi: 10.22034/iji.2023.96966.2473

Effects of Blocking NLRP3 Inflammasome on Type II Innate Lymphoid Cell Response in Allergic Rhinitis

Iranian Journal of Immunology
دوره 20، شماره 3، آذر 2023، صفحه 287-302    اصل مقاله (4.74 M)
نوع مقاله: Original Article
شناسه دیجیتال (DOI): 10.22034/iji.2023.96966.2473
نویسندگان
Guoqing Gong؛ Peng Huang؛ Changliang Yang؛ Chengcheng Huang؛ Zhao Zhang؛ Ruiyao Chen؛ Tingfeng Sun؛ Guang Yang*
Department of Otolaryngology, General Hospital of Central Theater Command, Wuhan, Hubei, China.
چکیده
Background: Type 2 innate lymphoid cells (ILC2s) and NLRP3 inflammasome are related to allergic and inflammatory responses. NLRP3 inflammasome inhibitor MCC950 was demonstrated to ameliorate allergic rhinitis (AR) in animal models.
Objective: To elucidate the effect of MCC950 on ILC2 responses in AR.
Methods: NLRP3 inflammasome, ILC2s, IL-5+ILC2s, IL-13+ILC2s, and Th2-related factors were examined in 30 AR patients. ILC2s were identified as Lin-CRTH2+CD127+lymphocytes. ILC2s isolated from PBMCs were stimulated with LPS plus ATP. The effect of MCC950, IL-1β, and IL-18 on ILC2 responses was detected by flow cytometry. AR models were established in 60 BALB/c mice. Nasal symptoms and ILC2 responses in the AR models after MCC950 treatment were detected. Human nasal epithelial cells were stimulated with IL-13 (10 ng/mL) and treated with MCC950 (10 μM).
Results: AR patients showed activated NLRP3 inflammasome and increased ILC2 responses compared to controls. NLRP3 inflammasome levels in the AR patients were positively related to the proportion of ILC2s, IL-5+ILC2s, and IL-13+ILC2s in total PBMCs. MCC950 treatment or IL-1β/IL-18 suppression inhibited ILC2 proliferation and Th2-related factors (GATA3, RORα, IL-5, and IL-13). MCC950 administration alleviated frequencies of nasal rubbing and sneezes in the AR models. ILC2s, IL-5+ILC2s, and IL-13+ILC2s in mice were reduced by MCC950. MCC950 inhibited NLRP3 inflammasome in the in vitro models of AR.
Conclusion: MCC950 inhibited ILC2 responses in AR and mice models, suggesting that blocking NLRP3 inflammasome may be a promising target for AR clinical treatment.
کلیدواژه‌ها
Allergic Rhinitis؛ MCC950؛ NLRP3 Inflammasome؛ Type II Innate Lymphoid Cell
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