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H. Tanioka, N. Yokoi, T. Shimamoto, A. Komuro, S. Kawasaki, A. Matsuda, S. Kinoshita; Composition of the Cornel Filament in Filamentary Keratitis on Immunohistochemical Examination. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2376.
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© ARVO (1962-2015); The Authors (2016-present)
It is reported that the corneal filament of filamentary keratitis is composed of epithelial cells and mucin through histological examination with a light microscope and an electron microscope. However, up until now, no studies have elucidated the composition of the filament in detail. In this experiment, we used an immunohistochemical technique to clarify the exact composition of the filament.
Filaments were obtained from13 filamentary keratitis patients with a background of post-penetrating keratoplasty, aqueous tear deficiency, and severe ocular surface disease who were receiving treatment at an outpatient facility. Transversal and longitudinal frozen-sections were prepared from those tissues, and subjected to an indirect fluorescent immunohistochemical analysis with primary antibodies including cytokeratin (CK1, CK4, CK6, CK10, and CK12), mucin (MUC1, MUC4, MUC5AC, and MUC16), keratinization-related protein (TGase 1 and fillagrin), desmoplakin, and markers of infiltration cells (CD3, HLA-DR, and neutrophil elastase). TUNEL staining was used for detection of apoptosis. Fluorescent images of the sections were inspected with a fluorescence microscope.
The filaments were composed of CK12-positive cells and had a roll-formed central core. They were covered with MUC5AC- and MUC16-positive mucin including CK4- and CK13-positive cells and neutrophil elastase-positive cells. The filaments also included broken cells and TUNEL-positive cells. However, those areas stained weakly for CK6 and HLA-DR, faintly for CK1, CK10, MUC1, MUC4 and CD3, and not at all for TGase 1, filaggrin, and desmoplakin.
We found that the filaments were composed of a roll-formed, corneal epithelium core covered with both gel-forming and membrane-associated mucin that included conjunctival epithelium, inflammation cells, and broken cells. We believe that the results of this research will open new pathways towards understanding the mechanism that generates the filament in filamentary keratitis, as well as new methods of treatment in the future.
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