Effects of Contact Lens Care Solutions on Surface Exfoliation and Bacterial Binding to Corneal Epithelial Cells1

Department of Ophthalmology, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390-9057, USA.
Eye & Contact Lens Science & Clinical Practice (Impact Factor: 1.47). 01/2003; 29(1):27-30. DOI: 10.1097/00140068-200301000-00008
Source: PubMed


The purpose of this study is to assess the effects of commercially available contact lens wetting solutions on bacterial binding and cell exfoliation rates in human corneal epithelium.
The effects of four contact lens care solutions were tested: ReNu Multi Plus (Bausch & Lomb, Rochester, NY) multipurpose solution; OPTI-FREE Express (Alcon, Ft. Worth, TX) multipurpose solution; Complete Blink-N-Clean (Allergan, Irvine, CA) lens drops; and Lens Plus (Allergan) rewetting drops.
Prospective, double-masked, randomized crossover clinical trial (N = 20 subjects).
Measures of outcome included binding of Pseudomonas aeruginosa (PA) to exfoliated corneal epithelial cells, and the rate of surface cell exfoliation. Cells were collected at the baseline (pretreatment) examination and 4 days later, after subjects used the assigned solution six times daily and once again immediately before cell collection (posttreatment). Following cell collection, patients underwent 1 week of recovery, during which no drops were used, and random cross-over assignment to the next test solution.
Use of test solutions increased PA binding, with a range of + 11.9% to + 58.2%. Analyzed together, PA binding increased significantly (+ 29%; P = 0.02, paired t-test); Lens Plus solution alone raised PA binding levels significantly (P = 0.022, 2-way ANOVA, Student-Newman-Keuls [SNK] test). Exfoliation rates were decreased from -7% to -52.7%. Analyzed together, cell exfoliation decreased significantly (P = 0.004; Wilcoxon signed rank test). Individual use of OPTI-FREE decreased exfoliation significantly (P = 0.019: 2-way ANOVA, SNK test).
Topical application of common commercial contact lens care solutions increases PA binding and reduces corneal surface cell exfoliation. Similar effects have also been reported with contact lens wear. Taken together, the data suggest that the use of lens solution itself may play a role in increasing PA binding to corneal epithelial cells and, hence, might potentially contribute inadvertently to increased risk for lens-related microbial keratitis.

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Available from: Walter Matthew Petroll, Oct 06, 2014
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    • "MPS toxic staining has been shown to be a risk factor for corneal inflammatory events, however, thus far there has been no correlation between staining and MK (Carnt et al 2007). Importantly, while no association has been established, the use of chemically preserved MPS in human clinical trials has been shown to reduce epithelial desquamation in concert with an upregulation of PA-binding receptors in surface epithelial cells in both the presence and absence of a contact lens (Li et al 2003). This increase in PA binding to corneal epithelial cells is a well-established risk factor for infection. "
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    ABSTRACT: Microbial keratitis (MK) is the most visually devastating complication associated with contact lens wear. Pseudomonas aeruginosa (PA) is highly invasive in the corneal epithelium and is responsible for more than half of the reported cases of contact lens-related MK. To protect against Pseudomonas-mediated MK, the corneal epithelium has evolved overlapping defense mechanisms that function to protect the ocular surface from microbial invasion. Research has shown that contact lens wear disrupts these protective mechanisms through breakdown of normal homeostatic surface renewal as well as damaging the corneal surface, exposing underlying cell membrane receptors that bind and internalize PA through the formation of lipid rafts. Human clinical trials have shown that initial adherence of PA with resulting increased risk for microbial infection is mediated in part by contact lens oxygen transmissibility. Recently, chemical preserved multipurpose solutions (MPS) have been implicated in increasing PA adherence to corneal epithelial cells, in addition to inducing significant levels of toxic staining when used in conjunction with specific silicone hydrogel lenses. This review summarizes what is currently known about the relationship between contact lenses, the corneal epithelium, MPS, and infection.
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    ABSTRACT: To investigate the effect of hypoxia-induced molecular responses of corneal epithelial cells on the surface of rabbit and human corneas and corneal cells in culture on interactions with Pseudomonas aeruginosa that may underlie increased susceptibility to keratitis. Organ cultures of rabbit and human corneal tissue, primary rabbit and human corneal cells, and transformed human corneal cells from a patient with cystic fibrosis and the same cell line corrected for expression of wild-type cystic fibrosis transmembrane conductance regulator (CFTR), the cellular receptor for P. aeruginosa, were exposed to hypoxic conditions for 24 to 72 hours. Changes in binding and internalization of P. aeruginosa were measured using cellular association and gentamicin-exclusion assays, and expression of CFTR and activation of NF-kappaB in response to hypoxia were determined by confocal laser microscopy and quantitative measurements of NF-kappaB activation. Hypoxia induced in a time- and oxygen-concentration-dependent manner increased association and internalization of clinical isolates of P. aeruginosa in all cells tested. Hypoxia increased CFTR expression and NF-kappaB nuclear translocation in rabbit and human cells with wild-type CFTR. Corneal cells lacking CFTR had reduced NF-kappaB activation in response to hypoxia. Hypoxia did not affect the increase in corneal cell CFTR levels or NF-kappaB activation after P. aeruginosa infection. Hypoxic conditions on the cornea exacerbate the binding and internalization of P. aeruginosa due to increased levels of CFTR expression and also induce basal NF-kappaB activation. Both of these responses probably exacerbate the effects of P. aeruginosa infection by allowing lower infectious doses of bacteria to induce disease and promote destructive inflammatory responses.
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