Abstract
BackgroundWe wanted to investigate whether parasympathetic inhibition affected the expression of type 2 innate lymphoid cells (ILC2s) in the nasal mucosa of a mouse model of allergic rhinitis (AR). MethodsThirty male C57BL/6 mice were randomly divided into 3 groups: control group, AR group, AR-treated group. AR nasal symptoms were assessed on a semi-quantitative scale according to the frequencies of nose rubbing and sneezing and the degree of rhinorrhea. The expression of cytokines protein in serum was detected by enzyme linked immunosorbent assay (ELISA). The number of ILC2s in nasal mucosa was detected by immunofluorescence double staining assay. Quantitative real-time Polymerase Chain Reaction (qPCR) was used to detect the expression of ILC2-associated factor in nasal mucosa. ResultsThe symptom scores of the AR group were significantly higher than those of the control group and AR-treated group. The expression levels of mouse ovalbumin (OVA) specific IgE, IL4, IL5, and IL13 in the serum of AR group were significantly higher than those in the control group and AR-treated group. The number of ILC2s and the gene expression of ILC2s related factors GATA3, CD25 and CD90 (Thy1) in the nasal mucosa of the AR group were significantly higher than those of the control group and AR-treated group. ConclusionsWe found that parasympathetic inhibition relieved AR symptoms and inhibited immune response of AR mice. ILC2s play an important role in the occurrence and development of AR, and parasympathetic nerve inhibition reduced the number of ILC2s and inhibited the cytokines expression by ILC2s. Our data provide information on the mechanism of action of parasympathetic inhibition in AR.
Highlights
Allergic rhinitis (AR), a non-infectious chronic inflammatory disease, affects 10%–20% of the global population and the proportion is still increasing.[1]
We found that parasympathetic inhibition relieved allergic rhinitis (AR) symptoms and inhibited immune response of AR mice
Type 2 innate lymphoid cells (ILC2s) play an important role in the occurrence and development of AR, and parasympathetic nerve inhibition reduced the number of ILC2s and inhibited the cytokines expression by ILC2s
Summary
Allergic rhinitis (AR), a non-infectious chronic inflammatory disease, affects 10%–20% of the global population and the proportion is still increasing.[1]. The excitement of the sensory nerve can cause nasal itching and sneezing, while the excitation of the parasympathetic nerve can stimulate glandular secretion and vasodilation, causing runny nose and other symptoms.[2] It has been found that mast cells directly contacted and attached to the nerve through cell adhesion molecule 1 (CADM1),[3,4] which kept increasing during inflammation of AR.[5,6] And eosinophils are found to accumulate around cholinergic nerves in allergic reactions.[7] The mediators secreted by neurons, including neuropeptides and neurotransmitters, act on the homologous receptors of allergic immune cells (mast cells, dendritic cells, eosinophils, Th2 cells, and ILC2s) to drive or regulate immunity.[8] In nasal mucosa, parasympathetic nerve has obvious functional advantages, while sympathetic nerve intervention has little effect on nasal mucosa inflammation.[9] it was found that ipratropium bromide, an anticholinergic drug, alleviated AR symptoms and reduced the number of eosinophils in nasal mucosa in a mouse model of AR.[10] All these studies show that the parasympathetic nerve plays an indispensable role in the occurrence and development of AR. We wanted to investigate whether parasympathetic inhibition affected the expression of type 2 innate lymphoid cells (ILC2s) in the nasal mucosa of a mouse model of allergic rhinitis (AR)
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