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M. Engelbert, M.S. Gilmore; Role of Innate Immune Privilege in Infection . Invest. Ophthalmol. Vis. Sci. 2003;44(13):1442.
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Purpose: To compare the course of infection with S. aureus in the immune privileged eye with the course of infection in the non-immune privileged, anatomically similar subcutaneous space in the ear. Methods: Eyes of 6 week old C57/BL6 mice received intravitreal injections of 5000 CFU S.aureus RN6390. Subcutaneous hyaluronic acid-filled blebs, which approximate the intraocular space with respect to its dimensions, but which are not subject to its immune regulation, were created by injecting 10 µl Restylane® crosslinked hyaluronic acid under the skin of mouse ears. After 1 week, these blebs were also infected with 5000 CFU S. aureus. Infections were allowed to progress for 12, 24, 48 and 96 hours, and eyes were collected for flow cytometric analysis and bacterial enumeration. Results: In the eye S. aureus rapidly grew from 5000 CFU at the time of infection to 1x109 CFU/ml by 24 hours, with little reduction in numbers by 96 hours, and complete organ destruction. In contrast, 5000 CFU S. aureus in subcutaneous blebs did not grow significantly over 96 hours after infection. Quantification of the inflammatory response by flow cytometry revealed that the inflammatory infiltrate in both sites at 24 hours consisted of similar amounts of CD45+ cells, predominantly Gr1+ neutrophils, despite a 4 log10 difference in bacterial numbers. A significantly greater number of ToPro-3+ dead cells was present in the eye. Discussion: Infection of the mouse eye with 5000 CFU S. aureus cannot be controlled by the host immune response and eventually results in destruction of the eye. An identical number of S. aureus in the subcutaneous space is well controlled by the immune system and smolders as a subacute infection. This shows that the innate immune response to infection is limited in the eye in the early phase of infection, either through inhibiting the robust induction of an immune response and/or hampering effector cell function. Dean A. McGee Eye Institute, Department of Ophthalmology and Department of Microbiology and Immunology, Oklahoma University Health Sciences Center, Oklahoma City, USA
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