TRPV1 regulates inflammatory process in the tongue of surgically induced xerostomia mouse.

BACKGROUND

The aim of study is to investigate the role of transient receptor potential cation channel subfamily V member 1 (TRPV1) on xerostomia-induced inflammatory response in vivo.

METHODS

Parotid, submandibular, and lingual gland were removed for xerostomia induction. The expression of inflammatory cytokines, TRPV1, NFkB, and MAPK in xerostomia was evaluated and compared in both TRPV1 wild and knockout mice.

RESULTS

The level of interleukin-6 (IL-6) and IL-17, neutrophil/CD4 T-cell infiltration, phosphorylation of extracellular signal-regulated kinase (ERK) and c-Jun N terminal kinase, TRPV1, and the localization of NFkB were elevated in xerostomia-induced TRPV1 wild-type mice. In contrast, inflammatory cytokines and MAPK were decreased in xerostomia-induced TRPV1 knockout mice. TRPV1 antagonist treatment also reduced tongue ulceration, neutrophil/CD4+ T-cell expression, IL-6, and IL-17 in TRPV1 wild-type mice.

CONCLUSION

TRPV1 had a crucial role in modulating inflammation in xerostomia and targeting TRPV1 might be a promising therapeutic strategy for xerostomia.