Vanadium inhalation effects on the corneal ciliary neurotrophic factor (CNTF): study in a murine model

Air pollution is a public health problem caused by predatory human activities and the indiscriminate burning of fossil fuels that liberate particulate matter (PM) into the atmosphere. Vanadium (V) adheres to them and reaches the bloodstream and different organs such as the eye when inhaled. Another way to reach the eye is by direct contact, and the cornea is the first layer exposed. Ciliary neurotrophic factor (CNTF) is secreted by the corneal nerves and some of its functions include self-renewal maintenance and wound healing by the activation of STAT3. Previous reports from our group indicate the activation of STAT3 after the inhalation of V, adhered to PM.

To analyse the effect of V inhalation in the expression of CNTF. Method: CD-1 male mice were exposed for 4 and 8 weeks to V inhalation. The eyes were removed, and the corneas were processed for immunohistochemistry for CNTF and analysed by densitometry. The same slides were used to evaluate histological modifications and to measure the corneas' anterior epithelial and endothelial thickness.

A decrease in CNTF expression in the anterior epithelium in the 8th week, as well as an increase in the endothelial and corneal thickness and disarray of all the layers of the anterior epithelium.

V inhalation disturbs the architecture of the cornea and modifies the presence of CNTF which might modify the renewal of the corneas after exposure to PM air pollution.