TRPM2 Deficiency Attenuates Allergic Rhinitis-Like Inflammation With Altered Ca2+-NFAT Signaling, Treg Responses, and sIgE Production.
Allergic rhinitis (AR) is a prevalent chronic inflammatory condition characterized by nasal itching, sneezing, and congestion, significantly impairing patients' quality of life. Despite the availability of various therapeutic options, treatment efficacy remains suboptimal for certain patients, and long-term use may be accompanied by adverse effects.
This study examined the role of transient receptor potential melastatin 2 (TRPM2) in AR-like inflammation, focusing on its associations with T cell functionality, Th2 inflammatory responses, Treg/Th17 balance, and upstream Ca2+-NFAT signaling pathways.
Using TRPM2 knockout and WT mice within an ovalbumin-induced AR model, this research integrated behavioral assessments, histopathological analyses, immunological assays, qPCR, and Western blotting to evaluate the implications of TRPM2 deficiency for clinical symptoms, inflammatory responses, immune cell differentiation, and related signaling pathways.
TRPM2 knockout mice exhibited reduced clinical symptoms and nasal inflammation, lower serum OVA-specific IgE levels, and reduced expression of key inflammatory cytokines, including IL-4, IL-5, and IL-33. Furthermore, TRPM2 deficiency was associated with expansion of Treg cells, reduced Ca2+ influx, decreased NFATc1 nuclear translocation, and lower IL-2 production. Although IL-17 expression was reduced, the decrease in Th17 cell frequency did not reach statistical significance.
These findings suggest that TRPM2 participates in OVA-induced AR-like inflammation through immune and Ca2+-NFAT-associated mechanisms, while the mechanistic and translational implications require cautious interpretation.
This study examined the role of transient receptor potential melastatin 2 (TRPM2) in AR-like inflammation, focusing on its associations with T cell functionality, Th2 inflammatory responses, Treg/Th17 balance, and upstream Ca2+-NFAT signaling pathways.
Using TRPM2 knockout and WT mice within an ovalbumin-induced AR model, this research integrated behavioral assessments, histopathological analyses, immunological assays, qPCR, and Western blotting to evaluate the implications of TRPM2 deficiency for clinical symptoms, inflammatory responses, immune cell differentiation, and related signaling pathways.
TRPM2 knockout mice exhibited reduced clinical symptoms and nasal inflammation, lower serum OVA-specific IgE levels, and reduced expression of key inflammatory cytokines, including IL-4, IL-5, and IL-33. Furthermore, TRPM2 deficiency was associated with expansion of Treg cells, reduced Ca2+ influx, decreased NFATc1 nuclear translocation, and lower IL-2 production. Although IL-17 expression was reduced, the decrease in Th17 cell frequency did not reach statistical significance.
These findings suggest that TRPM2 participates in OVA-induced AR-like inflammation through immune and Ca2+-NFAT-associated mechanisms, while the mechanistic and translational implications require cautious interpretation.