Abstract
The objective of this study is to analyze the expression of ILC2 cells (type 2 innate lymphoid cells) in nasal mucosa based on animal model of allergic bacterial infection rhinitis. 45 female BALB/c mice were selected as research subject. They were randomly divided into control group (group A), sensitization group (group B) and inhibitor group (group C) to establish a mouse model of allergic rhinitis. The pathological changes of mouse nasal mucosa were observed by HE (hematoxylin–eosin) staining. The number of ILC2 cells in mouse nasal mucosa was detected by immunofluorescence double staining assay. Real-time quantitative Polymerase Chain Reaction (PCR) was used to detect the expression of ILC2 cell-associated factor in mouse nasal mucosa. The expression of cytokine protein in serum was detected by enzyme linked immunosorbent assay. The results showed that there was no inflammatory cell infiltration in the nasal mucosa of group A, and the number of ILC2 cells was small. Inflammatory cell infiltration and obvious ILC2 cells were observed in the nasal mucosa of group B and C, and the number of ILC2 cells in group B and C was significantly increased compared with that in group A. Compared with group A, ROR α, Thy-1, ST2, and CD90 genes were significantly increased in nasal mucosa tissues of group B and C, and protein levels of IL-4, IL-5, IL-13, and IgE in serum were significantly increased. Compared with group B, the protein expression levels of IL-13 and IgE in serum of group C mice were significantly increased, while the expression levels of IL-4 and IL-5 were not significantly different. In conclusion, in the pathogenesis of allergic rhinitis, ILC2 cells play a role in promoting the development of inflammation, and its expression is related to RORα, Thy-1, ST2 and CD90. Meanwhile, ILC2 cells are also important cells for the synthesis and secretion of IL-13. The study on the pathogenesis of allergic rhinitis provides a new target for its treatment.
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