Reduction of collagen type I in the ciliary muscle of inflamed monkey eyes

PURPOSE. To investigate in monkey ciliary muscle the relationship between t he extent of anterior segment inflammation and alterations of collagen type I as determined by quantitative imaging densitometry. METHODS. Anterior segment inflammation was induced in one eye of five cynom olgus monkey by cannulation of the anterior chamber, by anterior chamber in jection of bovine serum albumin, or by disruption of the iris and anterior lens capsule with a needle. Increases in inflammatory cells were scored in hematoxylin and eosin-stained sections. Parallel eye sections were immunost ained for collagen type I and developed using diaminobenzidine. Optical den sity (OD) was measured along two line segments overlying the immunostained ciliary muscle using two-dimensional imaging densitometry. To assess antibo dy labeling of ciliary muscle structures, additional sections were double-i mmunostained using antibodies to collagen type I find calponin and examined by confocal microscopy. RESULTS. In each of the inflamed eyes, hematoxylin and eosin-stained sectio ns showed signs of chronic inflammation including lymphocytes and macrophag es dispersed among ciliary muscle fibers and in the iris. Double label conf ocal microscopy showed collagen type I immunoreactivity in the interstitial extracellular matrix between bundles of ciliary smooth muscle fibers. Coll agen type I OD scores in each of the inflamed eyes were less by 16% to 55%, compared with the contralateral control eyes. The mean of the OD scores fo r all inflamed eyes was 39% +/- 7% less than the mean of the control eye sc ores (mean +/- SEM, P < 0.001). Regression analysis showed a close correlat ion between inflammatory cell scores in the treated eyes and the reduction of OD scores (r = 0.94, P = 0.02). CONCLUSIONS. These results indicate that the density of collagen type I in the extracellular matrix (ECM) of monkey ciliary muscle is reduced during a nterior segment inflammation and support the view that reduction of ciliary muscle ECM may contribute to increased uveoscleral outflow facility during anterior segment inflammation.