Dry eye disease (DED) involves neurosensory abnormalities and inflammation. The aim of this study was to elucidate the role of transient receptor potential ankyrin-1 (TRPA1), a highly expressed corneal nociceptor, in neurogenic inflammation associated with persistent DED.Multi-unit extracellular recording of naive mice ciliary nerve was monitored with/without TRPA1 antagonist (HC030031), to determine which corneal nerve fiber is inhibited by this antagonist. DED was induced in mice by removing the extraorbital lacrimal gland and Harderian gland. Mice underwent topical treatment with HC030031 or vehicle, administered twice daily from d7 to d21 post-surgery. Corneal sensitivity and integrity (mechanical sensitivity, slit lamp, in vivo confocal microscopy (IVCM)) were monitored. Cornea and trigeminal ganglion (TG) were collected at d21 for protein and mRNA expression.Electrophysiological recordings showed that HC030031 had no effect on spontaneous neuronal activity but blocked the response to thermal stimulation. Behavioural assessment showed that corneal mechanical hypersensitivity and ocular discomfort induced by DED were both partially reversed by HC030031. In addition, HC030031 promoted corneal nerve regeneration in DED mice. Our data showed that HC030031 reduced inflammation in the cornea and TG. Indeed, HC030031 treatment led to a decrease in corneal immune cells observed with IVCM, and a decrease of corneal IBA1+ cells and IBA1+/CD68+ cells. Finally, HC030031 decreased inflammatory genes expression in the cornea (CCL2, IL1β) and TG (CX3CR1, CSF1, P2RX7…).In conclusion, our results indicate that TRPA1 corneal nociceptors, like TRPV1 or TRPM8, are important regulators of neurosensory abnormalities and neurogenic inflammation in the context of DED.