Contralateral inflammatory effects on the trigeminal ganglion after unilateral corneal lesion

Abstract

AbstractThe purpose of this study was to test whether a corneal injury can stimulate inflammation in the trigeminal ganglion (TG) located (i) on the same side, or (ii) on the opposite site of a cornea alkali burn.Following monolateral administration of a corneal alkali burn, we performed in vivo magnetic resonance imaging (MRI) of the brain before and after ultrasmall superparamagnetic iron oxide nanoparticle (USPIO) contrast to track macrophages. Trigeminal ganglia were stained for Prussian Blue and inflammatory cell markers. Moreover, the tissue levels of pro‐inflammatory cytokines Interleukin‐1β, TNF‐α, and VEGF were quantified on days 1, 4, and 8, and 4 days after corneal topical anti‐inflammatory treatment with 0.2% dexamethasone. The expression of Substance P and its receptor NK‐1R was measured in the TG on day 4.Corneal alkali burn induced leukocyte infiltration, including T cells, in the right TG at 4 and 8 days. In vivo MRI showed an increased contrast uptake in the right TG, which peaked at day 8. Prussian Blue(+) USPIO(+) macrophages were observed in the right TG and exhibited an M2 phenotype. The M2‐macrophage infiltration was preponderant in the TG after damage. The proinflammatory cytokines Substance P and NK‐1R were significantly increased in both the TGs. The expression of IL‐1β and VEGF‐A was significantly reduced in the right TG with dexamethasone treatment.Our data support: (i) bilateral onset of inflammation in the TG following ocular surface damage; (ii) involvement of the neuropeptide Substance P in the propagation of inflammation from the cornea to the TG through corneal nerves.