TRPA1 and TRPM8 in Allergic Rhinitis and Chronic Rhinosinusitis: Emerging Role in Neuroimmune Inflammation

Nasal hyperreactivity (NHR) is a core symptom of allergic rhinitis (AR) and chronic rhinosinusitis (CRS), frequently induced by cold stimuli. Accumulating evidence indicates that NHR is largely mediated by neuroimmune mechanisms rather than classical allergen-driven inflammation alone. Among the molecular sensors involved, the cold-sensitive transient receptor potential channels transient receptor potential ankyrin 1 (TRPA1) and transient receptor potential melastatin 8 (TRPM8) have emerged as key regulators linking environmental cold exposure to sensory nerve activation, neuropeptide release, and immune modulation. This review systematically summarizes the expression, functions, and neuroimmune mechanisms mediated by TRPA1 and TRPM8 in AR and CRS, with a particular focus on their roles in NHR. Furthermore, it discusses the therapeutic potential of targeting these channels to alleviate neurogenic inflammation and refractory nasal symptoms, aiming to provide new perspectives for understanding disease mechanisms and developing precise treatments.