4.6 Article

Comparison of Aqueous Levels of Inflammatory Mediators Between Toxic Anterior Segment Syndrome and Endotoxin-Induced Uveitis Animal Models

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Publisher

ASSOC RESEARCH VISION OPHTHALMOLOGY INC
DOI: 10.1167/iovs.14-15051

Keywords

toxic anterior segment syndrome; endotoxin-induced uveitis; prostaglandin E2 tumor necrosis factor-alpha

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Funding

  1. Korean Health Technology R&D Project, Ministry of Health & Welfare, Republic of Korea [HI13C0055]

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PURPOSE. To compare clinical findings and the aqueous levels of inflammatory mediators between toxic anterior segment syndrome (TASS) and endotoxin-induced uveitis (EIU) animal models and to evaluate the efficacy of systemic steroid pretreatment in both animal models. METHODS. Rats were used in this study. Ortho-phthalaldehyde solution was injected into the anterior chamber to produce TASS (n = 30), and lipopolysaccharide was injected into one hind footpad to produce EIU (n = 30). Clinical findings were evaluated under slit-lamp examination, and the aqueous levels of prostaglandin E2 (PGE2) and tumor necrosis factor-a (TNF-alpha) were measured 24 hours after these procedures. Twelve of the rats in each animal model were pretreated with intraperitoneal injection of dexamethasone for 4 days before the development of TASS and EIU. RESULTS. Corneal haze scores were significantly higher for TASS than EIU, but clinical scores for anterior uveitis were not different between the two animal models. Although aqueous levels of PGE2 were markedly increased in both animal models, PGE2 levels were significantly higher for TASS than for EIU. However, an increase in aqueous levels of TNF-alpha was observed only in EIU. Dexamethasone pretreatment reduced the corneal haze score and clinical score for anterior uveitis in both animal models and inhibited the increase in aqueous levels of PGE2 and TNF-alpha. CONCLUSIONS. Prostaglandin E2 and TNF-alpha in aqueous humor seem to be regulated differently in animal models of TASS and EIU. However, dexamethasone pretreatment improved the clinical findings and inhibited the increases in PGE2 and TNF-alpha in both animal models.

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