TRPA1 receptor is upregulated in human oral lichen planus

• Published in: Oral diseases Vol. 23; no. 2; pp. 189 - 198
• Main Authors: Kun, J, Perkecz, A, Knie, L, Sétáló, G, Tornóczki, T, Pintér, E, Bán, Á
• Format: Journal Article
• Language: English
• Published: Denmark Wiley Subscription Services, Inc 01.03.2017
• Subjects: ACE inhibitor; angiotensin II; Calcium Channels - analysis; Calcium Channels - genetics; Case-Control Studies; Female; Humans; hypertension; Hypertension - complications; Hypertension - genetics; Hypertension - metabolism; immunohistochemistry; Inflammatory diseases; Interferon-gamma - genetics; Keratosis - genetics; Keratosis - metabolism; Lichen Planus, Oral - complications; Lichen Planus, Oral - genetics; Lichen Planus, Oral - metabolism; Male; Mouth Mucosa - chemistry; Nerve Tissue Proteins - analysis; Nerve Tissue Proteins - genetics; Oral diseases; oral lichen planus; qPCR; RNA, Messenger - metabolism; transient receptor potential ankyrin 1; Transient Receptor Potential Channels - analysis; Transient Receptor Potential Channels - genetics; TRPA1 Cation Channel; tumor necrosis factor α; Tumor Necrosis Factor-alpha - genetics; Up-Regulation; transient receptor potential ankyrin 1; tumor necrosis factor α; angiotensin II; qPCR; immunohistochemistry; oral lichen planus; hypertension; ACE inhibitor
• ISSN: 1354-523X; 1601-0825; 1601-0825
• DOI: 10.1111/odi.12593

Objective Oral lichen planus (OLP) is a chronic inflammatory disease of unknown etiology with antigen‐specific and non‐specific mechanisms. Transient receptor potential ankyrin 1 (TRPA1) is a non‐selective cation channel activated by noxious stimuli such as oxidative stress products evoking pain and release of proinflammatory mediators from sensory nerve endings culminating in neurogenic inflammation. Extraneuronal TRPA1s, for example, on immune cells possess yet unknown functions. Subjects and Methods We studied the buccal mRNA expression (qPCR) and protein localization (immunohistochemistry) of TRPA1 receptors and key OLP mediator transcripts in oral mucosa samples of healthy volunteers (n = 9), OLP patients (n = 43), and OLP‐like hyperkeratotic patients (n = 12). Results We measured 27.7‐ and 25.5‐fold TRPA1 mRNA increase in OLP and OLP‐like hyperkeratotic patients compared to healthy controls. TRPA1 transcripts elevated 2.4‐fold in hypertensive OLP but not in hyperkeratotic patients compared to counterparts, reduced by 1.6‐fold by angiotensin‐convertase inhibitor intake. TRPA1 messenger RNA was more coexpressed with transcripts of tumor necrosis factor α than with interferon γ. Keratinocytes, macrophages but not T cells expressed TRPA1. Conclusions We provided evidence for the extraneuronal presence and upregulation of the proinflammatory TRPA1 receptor in buccal samples of patients with OLP. This may implicate the ion channel in the pathomechanism of OLP.