The Immunological Correlation With Adenoid Hypertrophy and Allergic Rhinitis in Children

ABSTRACT The purpose of this study was to investigate the infiltration of immune cells and cytokines in children with adenoid hypertrophy (AH) and allergic rhinitis (AR). A total of 70 children with AH who underwent adenoidectomies were enrolled in this study. Based on positive skin prick test (SPT) results and a clinical diagnosis of AR, the patients were categorized into two subgroups: patients with isolated AH and those with coexisting AH + AR. Total IgE, neutrophils, basophils, and eosinophils were compared between the two groups. Additionally, the count of eosinophils within adenoid tissues was determined via hematoxylin and eosin (H&E) staining. Th17/Treg and Th1/Th2 ratios were calculated and analyzed through flow cytometry. Real‐time quantitative PCR was used to detect related inflammatory cytokine expression in CD4 + T cells. Eosinophil counts were notably higher in the serum and adenoid tissues of the AH + AR group ( p = 0.037 and p = 0.0023, respectively) than in the AH‐only group. In the peripheral blood and adenoid tissues, the Th17/Treg ratio was significantly increased ( p = 0.001 and p = 0.0002, respectively), and the Th1/Th2 ratio was considerably decreased in the AH + AR group relative to the AH‐only group ( p = 0.000452 and p = 0.0001, respectively). Furthermore, IL‐2, TGF‐β1, and IFN‐γ mRNA expression and cytokine levels were decreased, whereas IL‐4, IL‐13, and IL‐17 levels were increased in adenoid tissues of the AH + AR group relative to those in the AH‐only group. The significant increase of eosinophil counts and levels of total IgE in adenoid tissues of atopic children, as well as in peripheral blood, indicates the role of local atopy in AH, which is similar to the immune characteristics of AR. The involvement of Th17/Treg and Th1/Th2 cell imbalance in allergen and inflammatory responses is linked to AH development, whereas altered expression of CD4 + T cell‐related inflammatory cytokines is associated with AH progression, suggesting that AR may be a risk factor for AH and providing a potential alternative explanation for AH pathogenesis.