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Query: UMLS:C0022568 (keratitis)
 5,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pseudomonas aeruginosa has emerged as an important causative agent of bacterial keratitis, a rapidly progressive ocular condition that may result in blindness. Secretory mucin forms the main constituent of the precorneal tear film, a three-layer film on the ocular surface protecting the underlying corneal epithelium from potential pathogens. The purpose of the present study was to compare mucin degradation mechanisms between ocular P. aeruginosa strains. Mucin degradation was assessed by agarose electrophoresis, lectin blotting, and size exclusion chromatography. The results indicate that certain P. aeruginosa strains (Paer12, ATCC 15442, 6294, and Paer25) had depleted mucin from the culture supernatant and that this was contingent on the inherent ability of these isolates to produce proteases. Non-protease-producing strains (Paer1 and Paer3) did not appreciably degrade mucin. Further, galactosidase, N-acetylglucosaminidase, and N-acetylgalactosaminidase activities were detected in some strains, suggesting the operation of further mechanisms of mucin degradation by P. aeruginosa. Mucin degradation by P. aeruginosa also seemed to be for the acquisition of nutrients, as a growth advantage was observed in mucin-depleting strains over nondepleting strains in the long term. It is postulated that the degradation of mucin serves to collapse the mucin barrier and its associated network containing antibacterial tear components and to provide energy for sustained bacterial growth.
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PMID:Mucin degradation mechanisms by distinct Pseudomonas aeruginosa isolates in vitro. 1450 Apr 75

The availability of the confocal microscope over the past decade has allowed clinicians and researchers to refine their understanding of the physiological and pathological basis of the ocular response to contact lens wear, and to discover previously unknown phenomena. Mucin balls, which form in the tear layer in patients wearing silicone hydrogel lenses, can penetrate the full thickness of the epithelium, leading to activation of keratocytes in the underlying anterior stroma. Epithelial cell size increases in response to all forms of lens wear, with lenses of higher oxygen transmissibility (Dk/t) interfering least with the normal process of epithelial desquamation. A higher density of Langerhans' cells is observed in the layer of the sub-basal nerve plexus among contact lens wearers, suggesting that contact lens wear may be altering the immune status of the cornea. Dark lines and folds are observed in the oedematous cornea in response to contact lens wear. Mechanical stimulation of the corneal surface, due to the physical presence of a contact lens, and the consequent release of inflammatory mediators, is the likely cause of reduced keratocyte density associated with lens wear. Highly reflective stromal 'microdot deposits' are observed throughout the entire stroma in higher numbers in lens wearers. 'Blebs' in the endothelium have a bright centre surrounded by a dark annular shadow; this appearance is explained with the aid of an optical model. The confocal microscope has considerable clinical utility in diagnosing Acanthamoeba and fungal keratitis. At the limbus, contact lenses can induce structural changes such as increases in basal epithelial cell size. An increased number of rolling leucocytes is observed in limbal vessels in response to low Dk/t lenses. It is concluded that the confocal microscope has considerable utility in contact lens research and practice.
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PMID:Contact lens-induced changes in the anterior eye as observed in vivo with the confocal microscope. 1749 98