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Apoptosis mediates decrease in cellularity during the regression of Arthus reaction in cornea.

N Ozaki¹, M Ishizaki, M Ghazizadeh

¹Department of Ophthalmology, Nippon Medical School, Tokyo, Japan. melo-k@komagome-hospital.bunkyo.tokyo.jp

The British Journal of Ophthalmology

|April 24, 2001

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Apoptosis drives the regression of inflammatory cells and new blood vessels in the cornea following an Arthus allergic reaction. This programmed cell death is key to understanding corneal disease healing mechanisms.

Area of Science:

Ophthalmology
Immunology
Cell Biology

Background:

The Arthus reaction in the cornea involves inflammation and new blood vessel growth.
During healing, these inflammatory cells and vessels normally regress.

Purpose of the Study:

To investigate if apoptosis (programmed cell death) mediates the regression of corneal inflammatory cells and neovascularization.
To clarify cellular mechanisms in corneal disease pathobiology.

Main Methods:

An Arthus-type allergic reaction was induced in rabbit corneas using bovine serum albumin (BSA).
Corneal tissues were collected at various time points (3-20 days).
Apoptosis was identified using in situ TdT-dUTP nick end labelling (TUNEL) and electron microscopy.

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Main Results:

Inflammatory cells (PMNs, plasma cells) and neovascularization were observed initially.
Corneal tissues showed increased apoptosis in endothelial cells and inflammatory cells over time.
Macrophages, PMNs, and myofibroblasts cleared apoptotic bodies.

Conclusions:

Regression of cellular infiltrates and microvessel endothelial cells in the Arthus reaction is apoptosis-dependent.
Apoptosis is a crucial cellular mechanism in the pathobiology and resolution of corneal diseases.