Fig. 1: Unilateral dry eye does not lead to corneal epitheliopathy in the contralateral eye in both WT and Trpv1KO mice.

a Working hypothesis: ocular TRPV1 activation is the initiating event of both trigeminal neuroinflammation and neurogenic inflammation in DED, and in turn, these processes worsen corneal neuropathy and, ultimately, ocular surface disease. b The right extraorbital lacrimal gland was excised in WT or Trpv1KO mice of both sexes, leading to unilateral DED. Thus, the right and left eyes are referred to as ipsilateral (Ipsi) and contralateral (Contra), respectively. Sham-operated animals were included as controls (Ct). c The tear production on day 5 as measured by phenol red paper-wetting length. d The cumulative data (left) and representative micrographs (right) of corneal dextran-fluorescein uptake in Ct and unilateral DED mice from both strains. Data are shown as the MFI calculated with ImageJ software (Materials and methods). e The representative micrographs (left) and number (right) of proliferating (Ki67⁺, green) cells within the epithelial basal layer of corneal wholemounts obtained 10 days after unilateral DED induction; E-cadherin (epithelial-specific) stained in red. All experiments were performed twice or more with six mice per group per experiment. To compare means, two-way ANOVA was used for d, e (strain and treatment) with Dunnett’s post hoc test. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. ns, not significant.