Immune sentinel function of nasal mucosal epithelial cells in allergic rhinitis: a review on barrier damage and inflammatory amplification loops regulated by calcium signalling

Allergic rhinitis (AR) is a prevalent chronic inflammatory disorder characterized by complex pathophysiological mechanisms. Nasal mucosal epithelial cells serve as crucial “immune sentinels” that detect allergens and initiate immune responses, thereby playing a pivotal role in disease progression. Intracellular calcium signaling, as a vital second messenger, regulates epithelial barrier integrity and modulates immune functions within these cells. This review summarizes current understanding of the immune surveillance role of nasal mucosal epithelial cells in AR, emphasizing the regulatory mechanisms of calcium signaling pathways in barrier disruption and the amplification of inflammatory cycles. Recent studies reveal that aberrant calcium signaling contributes to nasal epithelial barrier dysfunction and excessive activation of inflammatory cells, which perpetuate chronic inflammation and exacerbate symptom severity. By integrating emerging evidence on calcium-mediated cellular processes, this article highlights the critical involvement of calcium signaling in maintaining epithelial homeostasis and controlling inflammatory responses in AR. Understanding these mechanisms provides novel insights into the pathogenesis of AR and identifies potential therapeutic targets aimed at restoring epithelial barrier function and modulating inflammatory cascades, thereby offering new directions for clinical intervention.