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R.N. Lausch, R. Yin, S. Molesworth–Kenyon, J. Oakes; Role for IL–17R in HSV–1 Induced Corneal Opacity and Angiogenesis . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2786.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: We previously showed that interleukin 17 receptor (IL–17R) is expressed and functional on cultured mouse corneal fibroblasts. To assess what role this receptor and its ligand IL–17 may play in the HSV–1 infected cornea studies were conducted in mice with a disrupted IL–17R gene. Methods: IL–17R–/– mice and their C57BL/6 IL–17R+/+ counterparts were infected intracorneally with 2x104 PFU HSV–1 strain RE and followed for the development of corneal opacity and angiogenesis. HSV–1 growth was monitored by plaque assay and levels of proinflammatory mediator production were determined by ELISA. Results:During the first week post–infection but not thereafter corneal opacity in IL–17R–/– hosts was significantly elevated relative to that seen in wild type controls. Within this time frame HSV–1 titers were also higher in the IL–17R–/– hosts as were levels of the proinflammatory chemokines RANTES and MCP–1. In addition the production of IL–17 by draining lymph node cells was significantly reduced in the knockout mice. Interestingly, in week two of the infection the corneas of wild type mice manifested significantly greater angiogenesis than did the IL–17R–/– animals. This correlated with elevated levels of the proangiogenic factors VEGF, KC, and MIP–2. Conclusions:We conclude that IL–17 signaling through the IL–17R modulates host resistance against HSV–1 growth, and influences the development of both corneal opacity and angiogenesis.
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