Inflammation mechanism and anti-inflammatory therapy of dry eye

Abstract

Dry eye is a widespread chronic inflammatory disease that causes fatigue, tingling, burning, and other symptoms. Dry eye is attributed to rheumatic diseases, diabetes, hormone disorders, and contact lenses, which activate inflammatory pathways: mitogen-activated protein kinases (MAPK) and nuclear factor-B (NF-κB), promote macrophage inflammatory cell and T cell activation, and inflammation factors. Clinicians use a combination of anti-inflammatory drugs to manage different symptoms of dry eye; some of these anti-inflammatory drugs are being developed. This review introduces the dry eye inflammation mechanisms and the involved inflammatory factors. We also elucidate the anti-inflammatory drug mechanism and the detection limits.

Keywords: dry eye; inflammation; mechanism; review; therapy.

Figure 1

Inflammatory factors promote APC maturation. Mature APCs migrate through lymphatic vessels into regional lymph nodes with cytokines and chemokines. Additionally, it promotes naive T cells (Th 0) to form helper, memory, and regulatory T cells, which act on the ocular surface, secrete pro-inflammatory cytokines, and affect the corneal barrier function.

Figure 2

MAPK, VEGF, TGF-β, TNF, TLR-4 pathways in dry eye activated cells. Inflammation and VEGF activate MAPK, which generates JNK, P38, and ERK through ASK and Ras. TNF activates Ras and induces NF-κB production. TLR-4 activation induces ROS and inflammatory body production in cells. The TGF-β pathway binds and phosphorylates Smad2/3/4. The newly generated JNK, P38, ERK, NF-κB, and Smad2/3/4 in the cytoplasm enter the nucleus and affect the inflammatory gene expression.