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.

Objectives: We aimed to characterize the clinicopathologic features, treatment, and outcomes of three types of Switch/Sucrose Nonfermentable (SWI/SNF)-deficient sinonasal carcinomas (SDSCs), thereby expanding the spectrum of these rare entities and facilitating early diagnosis. Methods: We designed a retrospective single-center case series to analyze the clinicopathological features of 17 patients with SMARCB1-deficient sinonasal carcinoma (n = 10), SMARCA4-deficient carcinoma (n = 6) and SMARCA4-deficient sinonasal teratocarcinosarcoma (TCS) (n = 1) treated between 2018 and 2025, and reviewed the relevant literature. Results: The cohort included 14 males and 3 females, aged 26 to 69 years (mean, 47 years). SMARCB1-deficient sinonasal carcinomas predominantly involved the ethmoid sinus (6 of 8 patients), presenting epistaxis (7 of 10 patients), nasal obstruction (5 of 10 patients), and ocular symptoms (4 of 10 patients). SMARCA4-deficient sinonasal carcinomas mainly arose in the nasal cavity (3 of 4 patients), characterized by nasal obstruction (4 of 6 patients), and epistaxis or purulent rhinorrhea (4 of 6 patients); ocular symptoms were less common (2 of 6 patients). The TCS patient had left nasal cavity and ethmoid involvement with nasal obstruction and purulent rhinorrhea. Most patients presented with advanced-stage disease (T4a, n = 9), with skull base (n = 6), and orbital (n = 3) involvement. Histologically, immunohistochemical analysis confirmed complete SMARCB1 or SMARCA4 loss (complete in carcinomas and partial in TCS), diffuse CK positivity, and high Ki-67 indices. Treatment modalities included: chemotherapy and immunotherapy without surgery (n = 2), radical surgery with adjuvant chemoradiotherapy and immunotherapy (n = 2), radical surgery with chemoradiotherapy (n = 9), postoperative radiotherapy alone (n = 3), and non-radical surgery with chemoradiotherapy (n = 1). At a median follow-up of 19 months (range, 8–57 months), 2 patients were lost to follow-up, 3 died, 2 had persistent disease, and 10 remained disease-free. Conclusions: SDSC is an aggressive tumor with male predominance and advanced-stage presentation. Early recognition and appropriate immunohistochemical evaluation are essential for timely diagnosis and management. Prospective studies of novel targeted and immunotherapeutic strategies are warranted.