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E.A. Szliter, Y. Zhang, R.P. Barrett, M.M. Gabriel, L.D. Hazlett; Rat Extended Wear Contact Lens Model: Early Analysis of Pseudomonas aeruginosa–Induced Keratitis . Invest. Ophthalmol. Vis. Sci. 2005;46(13):5085.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: The purpose of this study was to examine the host response to P. aeruginosa–induced keratitis. A newly developed rat model of extended contact lens (CL) wear in which the cornea is not wounded, a requisite for all other rodent models, was used. Methods: Lewis rats were fitted with a soft CL (CIBA Vision, Duluth, GA) in the left eye, while the right eye served as a control and the lenses worn for three weeks before bacterial challenge. Infection routinely was induced in the experimental eye by placement of a bacterial–soaked CL (1 hour at 1.0 X 108 cfu) and then topical delivery (X1) of bacteria (10 µl; 1 X 108 cfu) 4 hours later. Upon detection of corneal opacity (24 hours), slit–lamp, histopathology, plate counts, ELISA, myeloperoxidase (MPO) for PMN quantitation, ADPase staining for Langerhans cell (LC) quantitation and RPA to detect mRNA of pro–inflammatory cytokines were done. In addition, at 48 hours after detection of corneal opacity, plate counts also were done. Results: Analysis of bacterial–induced keratitis in CL–wearing rats revealed an early (24 hours after challenge), host inflammatory response, albeit in the absence of detectable bacteria in the cornea. However, after an additional 24 hours, bacteria were readily detectable in the cornea. Overall, early (24 hours) disease also was evidenced by the proliferation and migration of LC and infiltration of PMN into the infected cornea with resultant corneal opacity. CL wear alone did not induce such cell infiltration. RPA and ELISA analyses also showed an up–regulation at mRNA and protein levels for cytokines IL–1ß and IL–6 at 24 hours after disease onset, further suggesting that with CL wear, the host inflammatory response has a major contribution to early corneal pathology. The data also suggest that the host response, including corneal epithelial edema and cell infiltrate, induced by the presence of bacteria on the CL, allows the bacteria to breach the dysfunctional epithelial barrier and grow within the cornea, given sufficient time. Conclusions: Although this model requires a large bacterial inoculum and repeated challenge to induce infection, it provides new information about the early effects of CL usage and suggests the importance of the host response to facilitate corneal changes that favor bacterial invasion and subsequent infection. As it does not require trauma, usually needed for all other rodent models, the rat model should prove valuable for delineation of the effects of CL wear in infectious and other CL–related complications and diseases.
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