CXCL16 deficiency alleviates ovalbumin-induced allergic rhinitis in mice.

Abstract

PURPOSE: Research has indicated that individuals with allergic rhinitis exhibit elevated levels of CXCL16 expression in their serum. This study aims to illustrate the role of CXCL16 and its associated mechanisms in mice suffering from allergic rhinitis. METHODS: An allergic rhinitis model was established by injecting ovalbumin (OVA) into mice, and the expression of CXCL16 mRNA and protein in nasal mucosal tissue was measured. The frequency of nose rubbing and sneezing in each group of mice was recorded. Serum levels of IgE and IgG1 were also assessed. Th2 cell-related factors in the bronchoalveolar lavage fluid (NALF) were analyzed. Histological staining was used to examine pathological changes in the nasal and lung tissues. The expression levels of p-p65, p65, p-IκBα, and IκBα proteins in nasal tissues were evaluated using western blot. RESULTS: CXCL16 expression was elevated in OVA-induced allergic rhinitis mice. CXCL16 knockout reduced the frequency of nose wiping and sneezing in OVA-induced mice and suppressed the levels of IgE and IgG1. Furthermore, CXCL16 knockout led to a decrease in both the number of inflammatory cells and the levels of inflammatory factors in NALF. Histological staining revealed that CXCL16 knockout alleviated pathological tissue changes and goblet cell hyperplasia. Additionally, CXCL16 knockout suppressed the expression of p-p65/p65 and p-IκBα in nasal tissues, while increasing the expression of IκBα. CONCLUSION: CXCL16 deficiency alleviates allergic rhinitis.