Investigating the inflammatory cascade effect of basophil activation in children with allergic rhinitis or asthma, via the IgE-FcεRI-NF-κB signaling pathway.

Abstract

Allergic rhinitis (AR) is a type I allergic reaction mediated by serum immunoglobulin E (IgE). This study aimed to investigate the basophil activation rate and serum expression of inflammatory factors in AR patients and rats. The involvement of the IgE-FcεRI-nuclear factor kappa B (NF-κB) signaling pathway in the pathogenesis of AR was also explored. Thirty patients with pediatric AR (or asthma; untreated) were enrolled in our hospital as the observation group. Fifteen healthy children were selected as the control group. The basophil activation and serum levels of interleukin (IL)-4, IL-5, IL-13, IgE, and prostaglandin D2 (PGD2) in 2 groups of children were detected. Forty-eight male Sprague Dawley rats were randomly divided into group A (AR model group), group B (AR model + IgE inhibitor), group C (AR model + omalizumab), and group D (control). The animal model was established by intraperitoneal injection of ovalbumin and nasal mucosa stimulation. The basophil activation rate, serum levels of IL-4, IL-5, IL-13, IgE, and PGD2 were analyzed. In children with AR, the blood samples contained mainly activated basophils, whereas the healthy group showed mainly non-activated basophils. The levels of IL-4, IL-5, IL-13, IgE and PGD2 in the serum of the AR group were higher than those in healthy subjects (p < 0.05). In animal studies, the blood samples collected from group A were mainly activated basophils, while the samples of the other groups were mainly non-activated basophils. The serum contents of IL-4, IL-5, IL-13, IgE, and PGD2 in group A were significantly higher than those in groups B and C (p < 0.05). Patients with AR showed increased activation of basophils and elevated expression of IL-4, IL-5, IL-13, IgE, and PGD2. The upregulation of FcεRI and NF-κB was involved in the pathogenesis of AR.