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Yan Sun, Jyotsna Chandra, Pranab Mukherjee, Loretta Szczotka-Flynn, Mahmoud A. Ghannoum, Eric Pearlman; A Murine Model of Contact Lens–Associated Fusarium Keratitis. Invest. Ophthalmol. Vis. Sci. 2010;51(3):1511-1516. doi: https://doi.org/10.1167/iovs.09-4237.
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Fusarium solani and F. oxysporum were the causative organisms of the 2005/2006 outbreak of contact lens–associated fungal keratitis in the United States. The present study was an investigation of the ability of F. oxysporum grown as a biofilm on silicone hydrogel contact lenses to induce keratitis.
A clinical isolate of F. oxysporum was grown as a biofilm on lotrafilcon A contact lenses, and a 2-mm diameter punch was placed on the abraded corneal epithelium of either untreated or cyclophosphamide-treated C57BL/6 mice or of IL-1R1−/−, MyD88−/−, TLR2−/−, or TLR4−/− mice. After 2 hours, the lens was removed, and corneal opacification, colony forming units (CFUs), and histopathology were evaluated.
C57BL/6 mice developed severe corneal opacification within 24 hours and resolved after four days. In contrast, corneal opacification progressed in cyclophosphamide-treated mice, and was associated with unimpaired fungal growth in the cornea, and with hyphae penetrating into the anterior chamber. The phenotype of MyD88−/− and IL-1R−/− mice was similar to that of cyclophosphamide-treated animals, with significantly impaired cellular infiltration and fungal clearance. Although TLR4−/− mice developed a cellular infiltrate and corneal opacification similar to C57BL/6 mice, the CFU count was significantly and consistently higher.
Fusarium grown as a biofilm on silicone hydrogel contact lenses can induce keratitis on injured corneas, with disease severity and fungal killing dependent on the innate immune response, including IL-1R1, MyD88, and TLR4.
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