Abstract
Purpose :
To evaluate corneal endothelial cell number and the expression of neurokinin-1 receptor (NK1R) in the endothelium in normal vs. ocular GVHD (oGVHD) corneas and to correlate the density of endothelial cells with clinical and histological inflammatory parameters.
Methods :
Pre-conditioning was performed in BALB/c using myeloablative total body irradiation. Subsequently, allogeneic bone marrow transplantation was infused without (BM, n=8) or with mature T cells (BM + T, n=8). BM and normal wild type mice (n=7) were used as controls. Corneal transparency and blepharitis were assessed at the end of the experiment (day 29). After sacrifice, endothelial cell number, corneal thickness, and CD3+ cells were quantified, and the expression of NK1R was investigated in the corneal endothelium through immunofluorescence and quantified by immunohistochemistry.
Results :
oGVHD mice showed a significant reduction in the endothelial cell number compared to controls (p<0.0001). In addition, NK1R expression was found in the endothelium, and it was significantly increased in oGVHD vs. control mice (p<0.05). Corneal transparency and thickness remained unchanged in all groups. An inverse correlation was found between endothelial cell number and the CD3+ cell infiltrate (Pearson r= -0.8712, p<0.05) and with blepharitis severity (Pearson r= -0.5959, p<0.01).
Conclusions :
Our findings suggest that oGVHD is associated with reduced corneal endothelial cell density and increased expression of endothelial NK1R. Corneal endothelial cell loss correlates with increased expression of clinical and histological markers of inflammation.
This abstract was presented at the 2022 ARVO Annual Meeting, held in Denver, CO, May 1-4, 2022, and virtually.