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Thermosensitive transient receptor potential (TRP) ion channels expressed in the dental pulp may be key transducers of inflammation and nociception. We aimed at investigating the expression and role of thermo\u2010TRPs in primary human dental pulp cells (hDPCs) in normal and inflammatory conditions.<\/jats:p><\/jats:sec><jats:sec><jats:title>Experimental Approach<\/jats:title><jats:p>Inflammatory conditions were induced in hDPC cultures by applying polyinosinic:polycytidylic acid (poly(I:C)). Gene expression and pro\u2010inflammatory cytokine release were measured by RT\u2010qPCR and ELISA. Functions of TRPA1 channels were investigated by monitoring changes in intracellular Ca<jats:sup>2+<\/jats:sup> concentration. Mitochondrial superoxide production was measured using a fluorescent substrate. Cellular viability was assessed by measuring the activity of mitochondrial dehydrogenases and cytoplasmic esterases. TRPA1 activity was modified by agonists, antagonists, and gene silencing.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key Results<\/jats:title><jats:p>Transcripts of TRPV1, TRPV2, TRPV4, TRPC5, and TRPA1 were highly expressed in control hDPCs, whereas TRPV3, TRPM2, and TRPM3 expressions were much lower, and TRPM8 was not detected. Poly(I:C) markedly up\u2010regulated TRPA1 but not other thermo\u2010TRPs. TRPA1 agonist\u2010induced Ca<jats:sup>2+<\/jats:sup> signals were highly potentiated in inflammatory conditions. Poly(I:C)\u2010treated cells displayed increased Ca<jats:sup>2+<\/jats:sup> responses to H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>, which was abolished by TRPA1 antagonists. Inflammatory conditions induced oxidative stress, stimulated mitochondrial superoxide production, resulted in mitochondrial damage, and decreased cellular viability of hDPCs. This inflammatory cellular damage was partly prevented by the co\u2010application of TRPA1 antagonist or TRPA1 silencing.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion and Implications<\/jats:title><jats:p>Pharmacological blockade of TRPA1 channels may be a promising therapeutic approach to alleviate pulpitis and inflammation\u2010associated pulpal damage.<\/jats:p><\/jats:sec>","DOI":"10.1111\/bph.16386","type":"journal-article","created":{"date-parts":[[2024,5,15]],"date-time":"2024-05-15T02:56:36Z","timestamp":1715741796000},"page":"3246-3262","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["TRPA1 up\u2010regulation mediates oxidative stress in a pulpitis model in vitro"],"prefix":"10.1111","volume":"181","author":[{"given":"\u00c1rp\u00e1d","family":"Kunka","sequence":"first","affiliation":[{"name":"Department of Physiology, Faculty of Medicine University of Debrecen  Debrecen 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