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A Hypothalamic-Controlled Neural Reflex Promotes Corneal Inflammation.

Romina Mayra Lasagni Vitar¹, Philippe Fonteyne¹, Linda Chaabane²

¹Cornea and Ocular Surface Disease Unit, Eye Repair Lab, IRCCS San Raffaele Scientific Institute, Milan, Italy.

Investigative Ophthalmology & Visual Science

|October 26, 2021

Summary

This summary is machine-generated.

Corneal injury triggers a reflex involving substance P (SP) nerves, activating the hypothalamus and sympathetic system, leading to inflammation. SP depletion reduces this inflammatory response and improves corneal healing.

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Published on: November 22, 2024

Area of Science:

Neuroscience
Ophthalmology

Background:

Corneal injury can initiate inflammatory responses.
The role of sensory nerves and the central nervous system in corneal inflammation is not fully understood.

Purpose of the Study:

To investigate if acute corneal injury activates a proinflammatory reflex.
To determine the involvement of corneal sensory nerves expressing substance P (SP), the hypothalamus, and the sympathetic nervous system in this reflex.

Main Methods:

Mice (wild-type and SP-depleted) underwent corneal alkali burn.
Neuronal activation was assessed using cFOS staining and MRI.
Expression of key proteins (TH, NK1R, nNOS) and sympathetic activation (SCG, NA levels) were evaluated.
Corneal inflammation and transparency were monitored.

Main Results:

Alkali burn induced significant neuronal activation in the trigeminal ganglion and hypothalamus, which was reduced in SP-depleted mice.
SP depletion decreased presympathetic neuron activation, sympathetic neuron activation in the SCG, and noradrenaline levels.
Mice lacking SP showed reduced corneal leukocyte infiltration, opacity, and inflammation post-injury.

Conclusions:

Corneal sensory nerves containing SP activate hypothalamic presympathetic neurons, leading to sympathetic activation and corneal inflammation.
Targeting the SP pathway may offer a therapeutic strategy for managing corneal inflammation and promoting healing.