Idiopathic and allergic rhinitis show a similar inflammatory response

Abstract

HYPOTHESIS: Idiopathic and allergic rhinitics have similar mucosal mast cell and IgE+ cell distribution. INTRODUCTION: The pathophysiology of idiopathic rhinitis (IR) is unknown but patients differ from those with allergic rhinitis (AR) in that they do not express IgE. Our study is novel because we investigated: (1) three study groups chosen prospectively using strict selection criteria over a 4-year period; and (2) mast cell and IgE+ cell counts were on full-thickness, full-length inferior turbinate mucosa. METHODS: Patient groups: allergic (n = 17); idiopathic: (n = 16); and normal controls (n = 9). Immunohistochemistry: mast cell and IgE+ cell detection using anti-mast cell tryptase and anti-IgE antibodies with an avidin-biotin (peroxidase) complex on paraffin processed tissue. Morphometry: sections were divided into three strata comprising an epithelial layer and two submucosal layers. Statistics: Mann-Whitney non-parametric analysis. alpha = 0.05, beta = 0.2. RESULTS: The power of the study was 89%. Mast cells (P = 0.03) and IgE+ cells (P < 0.05) were significantly increased in the epithelium of idiopahtic and allergic rhinitis mucosa compared to the normal control. More IgE+ cells were counted in the AR and IR groups compared to the controls in all three strata. CONCLUSION: Mast cells and IgE+ cells are involved in the pahtophysiology of IR. We propose that IR may be a variant form of AR involving a localized IgE-mediated inflammatory response.

Association between SP‐A rs1965708 gene polymorphism and allergic rhinitis risk in Chinese population

“…The activation of these cytokines reflects the acute phase of the inflammatory response and has important consequences for the clinical manifestations of AR. 29 Our results also showed that the rs1965708 variants were associated with IgE and inflammation factors.…”

“…The pathogenesis of AR is related to the activation of circulating T lymphocytes and mononuclear macrophages, and its activation is related to cytokines such as IL‐1, TNF‐α, and IL‐6. The activation of these cytokines reflects the acute phase of the inflammatory response and has important consequences for the clinical manifestations of AR 29 . Our results also showed that the rs1965708 variants were associated with IgE and inflammation factors.…”

The paradigm of cytokine networks in allergic airway inflammation

“…They are produced and released by a wide variety of cell types, including immune cells like macrophages, B and T lymphocytes, and mast cells, as well as structural cells like endothelial cells, fibroblasts, and epithelial cells. In turn, these chemokines and cytokines are implicated in the migration of other inflammatory cells, as in the case of normal T-lymphocyte expressed (RANTES) and transforming growth factor (TGF)-beta regulated upon activation, which are implicated in the intraepithelial migration of mast cells [6,7]. The inflammatory process underlying allergic rhinitis and asthma is coordinated by a cytokine network.…”

International consensus statement on allergy and rhinology: Allergic rhinitis – 2023

“…IgE crosslinking results in mast cell activation and release of inflammatory cytokines such as IL‐4, IL‐5, IL‐6, IL‐13, IL‐25, and IL‐33 as well as preformed bioactive mediators and newly formed mediators including histamine, leukotrienes, prostaglandins, and kinins. These cytokines regulate the allergic inflammatory cascade through induction of IgE synthesis, upregulation of IgE production, and production of other cytokines and chemokines from epithelial cells which results in the mucosal recruitment of inflammatory cells 537–539 . Numerous cell types act as sources for type 2 cytokines including T cells, nasal epithelial cells, ILC2s, mast cells, and eosinophils.…”