先天性淋巴细胞
粒体自噬
自噬
帕金
炎症
免疫学
鼻粘膜
免疫球蛋白E
过敏性炎症
病理
生物
医学
抗体
先天免疫系统
免疫系统
细胞凋亡
疾病
生物化学
帕金森病
作者
Chen Wang,Zhuo Jia,Wenqian Li,Min-Li Zhou,Ke‐Jia Cheng
标识
DOI:10.1016/j.waojou.2023.100852
摘要
Roles of ILC2s in allergic rhinitis (AR) and local allergic rhinitis (LAR) are unclear. In this study, we are determined to find the levels of autophagy and mitophagy of ILC2s in allergic nasal inflammation.ELISA was used to detect type 2 inflammatory cytokines. Hematoxylin and eosin (H&E) staining were used to compare the eosinophil (EOS) infiltration of nasal tissue specimens. Flow cytometry was used to detect the levels of ILC2s and Th2 cells. Immunohistochemistry (IHC) and Western blot (WB) were used to detect the levels of Beclin1, LC3, p62, PINK1, Parkin, FUNDC1, and BNIP3 in nasal mucosa. The levels of autophagy related proteins and mitophagy related proteins of the ILC2s were detected by WB. The number of autophagosomes of ILC2s was observed by transmission electron microscopy. The co-localization levels of GFP-LC3 and Mito tracker in ILC2s were observed by confocal microscopy using immunofluorescence.We found that the level of type 2 inflammation in AR and LAR mice was significantly increased. The levels of autophagy and mitophagy of AR and LAR mice in nasal mucosa and ILC2s were both increased.ILC2s may be associated with the occurrence and development of nasal allergic inflammation. The abnormal increase of autophagy and mitophagy levels in the nose may be associated with the incidence of AR and LAR. Abnormal autophagy and mitophagy levels of ILC2s cells may be one of the causes of allergic nasal inflammation.
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