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Elena Koudouna, Naoki Okumura, Shinichiro Nakano, Ryota Inoue, Nigel Fullwood, Yugo Okazaki, Shigeru Kinoshita, Noriko Koizumi; Existence of inflammatory cells on donor corneal endothelium in a Descemet’s stripping automated endothelial keratoplasty rabbit model. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):4022.
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The loss of corneal endothelial cell (CEC) density continues post corneal transplantation, even in cases with successful clinically outcomes. Although reoperations are sometimes required, the pathophysiology of cell density loss has yet to be fully elucidated. The purpose of this present study was to establish a Descemet’s stripping automated endothelial keratoplasty (DSAEK) animal model and investigate the involvement of inflammatory cells post DSAEK.
As a DSAEK rabbit model, an 8-mm diameter of Descemet’s membrane was first stripped and microkeratome-produced corneal grafts from rabbit eyes were then transplanted in accordance with the standard DSAEK procedure in 20 eyes of 20 rabbits. Slit-lamp examination and contact specular microscopy was performed for 14-days postoperative. Corneal specimens were evaluated by scanning electron microscopy (SEM) and also immunostained for antibodies against CD3 (T cells), CD4 (T helper cells), CD8 (cytotoxic T cells), CD20 (B cells), and CD68 (macrophages) after 14 days.
In all eyes, corneal clarity was recovered within 7 days post DSAEK. No severe complications such as a failed graft, graft dislocation, or graft rejection were observed for 14-days postoperative. Contact specular microscopy showed a hexagonal monolayer of corneal endothelium over the whole area of the donor graft and host cornea. SEM showed that the grafts were attached onto the host corneal stroma. Moreover, inflammatory cell-like morphology was evident on the donor corneal endothelium, while few cells were observed on the peripheral host corneal endothelium. Immunohistochemical analysis demonstrated the existence of CD3-, CD4-, CD8-, CD20-, and CD68-positive cells on the donor corneal endothelium. Three-dimensional images revealed that those inflammatory cells were adhered onto the donor corneal endothelium and located at the anterior chamber side.
The findings of this study showed the existence of numerous inflammatory cells on donor corneal endothelium in a clinically successful DSAEK rabbit model. Although further study is needed to elucidate the pathophysiology of cell density loss post corneal transplantation, investigation of the involvement of inflammatory cells is important.
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