Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022568 (keratitis)
 5,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Extracellular proteases of three cornea-virulent strains of Pseudomonas aeruginosa were isolated by sequential ammonium sulfate precipitation, Ultrogel AcA 54 gel filtration, and flat-bed isoelectric focusing. The purity of the preparations was determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis , thin-layer isoelectric focusing in polyacrylamide gel, immunodiffusion and immunoelectrophoretic procedures, and tests for the presence of other known pseudomonal products. Light and electron microscopic examination of rabbit corneal lesions observed 4 to 6 h after the intracorneal injection of submicrogram amounts of the proteases revealed: (i) degeneration and necrosis of epithelium, endothelium, and keratocytes, (ii) infiltration, degeneration, and necrosis of polymorphonuclear leukocytes, (iii) loss of the characteristic weblike pattern, colloidal iron staining, and ruthenium red staining of the stromal proteoglycan ground substance, (iv) dispersal of strucutrally normal appearing collagen fibrils, ground substance, (iv) dispersal of structurally normal appearing collagen fibrils, and (v) accumulation of plasma proteins and fibrin in the necrotic corneas. These structural alterations are very similar to those observed previously during experimental P. aeruginosa keratitis, and this similarity supports the idea that pseudomonal proteases are responsible, at least in part, for the rapid and extensive liquefaction necrosis characteristic of pseudomonal-induced keratitis. In addition, the results support the idea that pseudomonal proteases elicit severe corneal damage by causing the loss of the corneal proteoglycan ground substance, thus resulting in dispersal of undamaged collagen fibrils, weakening of the corneal stroma, and subsequent descemetocele formation and corneal perforation by the anterior chamber pressure.
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PMID:Purification of Pseudomonas aeruginosa proteases and microscopic characterization of pseudomonal protease-induced rabbit corneal damage. 41 81

The structural alterations elicited in the rabbit corneal stroma by experimental Serratia marcescens keratitis and by a highly purified serratia protease preparation were compared by gross observation, biochemical analyses, and electron microscopic examination of the affected tissue. Acute inflammation, liquefactive necrosis of the cornea, and descemetocele formation occurred during the development of the infection and after the intracorneal injection of submicrogram amounts of the protease. In vitro incubation of insoluble corneal stromal tissue with the bacterium or with the protease resulted in solubilization of the stromal proteoglycan ground substance; however, specific collagenase activity was not detected. Electron microscopic examination of corneas damaged by the bacterial infection and by the protease revealed loss of ruthenium red staining of the proteoglycan ground substance and dispersal of ultrastructurally normal collagen fibrils. Thus, our findings indicate that the major corneal damage which occurs during serratia keratitis and after the injection of the serratia protease is caused by solubilization and loss of the ground substance of the tissue. In addition, the observation that the major structural alterations observed during serratia keratitis can be reproduced by the bacterial protease supports the idea that the enzyme is involved, at least in part, with the production of severe corneal damage by the bacterium.
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PMID:Characterization of rabbit corneal damage produced by Serratia keratitis and by a serratia protease. 702 49

Lumican is keratan sulfate proteoglycan of the small leucine rich proteoglycan family. Through studies in animal models lumican has been found to be critical in maintaining corneal clarity. It maintains ordered collagen fibrils which are vital in keeping the cornea transparent. It may also be important in primary open angle glaucoma influencing aqueous outflow. Lumican deficiency in mice results in increased axial length with fibromodulin deficiency and thinner sclerae. There is evidence suggesting that this characteristic may be pertinent in humans and lumican gene polymorphisms could be related to high myopia. Lumican plays a fundamental role in inflammation and wound healing. It localises macrophages to the site of corneal injury and recruits neutrophils in lipopolysaccharide-induced keratitis in mice. It has also been shown to bind lipopolysaccharide which may be critical in inflammatory diseases such as uveitis. Lumican is also important in wound healing revealing decreased synthesis in scar tissue and mediating Fas-Fas ligand interactions. It is present in human placenta and amniotic membrane suggesting that it may ensure viable amniotic membrane grafts. Lumican may also be involved in the formation of posterior capsular opacification following cataract surgery. Research into the pivotal role of lumican in the pathogenesis of ocular disease has resulted in greater understanding of the key role which proteoglycans play in human disease.
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PMID:The role of lumican in ocular disease. 2455 2