Objective The warm sensors located in keratinocytes have the ability to directly detect warm temperature, with TRPA1 in dorsal root ganglion (DRG) neurons being a potential mediator of the downstream transduction process. The present study aimed to elucidate the mechanism by which warm information is transmitted from keratinocytes to TRPA1.Methods TRPA1-transfected HKE293T cells as well as DRG neuron cells from wild-type and TRPA1 knockout mice were cultured separately, and stimulated with warm temperatures using a perfusion apparatus. Single cell calcium imaging was used to monitor calcium influx during stimulation, and the role of H₂O₂ in this process was also examined. Additionally, RNA-seq analysis was performed on primary keratinocytes cultured at different temperatures to identify potential candidates responsible for keratinocytes-TRPA1 warm transduction.Results Our finding indicated that TRPA1-transfected HEK293T cells or DRG neurons could be activated by warm temperature in the presence of H₂O₂. However, when TRPA1 was knocked out or blocked by HC-030031, the H₂O₂-potentiated warm response was significantly reduced. Moreover, Chemokine C—C motif ligand 2 (CCL2) and decorin (DCN), two H₂O₂ related factors, exhibited different expression patterns in keratinocytes cultured at 33℃ and 37℃, respectively. This result is consistent with previous research showing that mice stimulated at 37℃ induced more DRG activation than those stimulated at 33℃.Conclusion H₂O₂ can potentiate the TRPA1-dependent warm response, and H₂O₂-related factors in keratinocytes can be affected by warm temperature, suggesting the possible role of H₂O₂ related factors in warm transduction from keratinocytes to downstream TRPA1 in DRG neurons.