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IL-2 and IFN-gamma in the retina of diabetic rats.

Authors: Johnsen-Soriano, S  Sancho-Tello, M  Arnal, E  Navea, A  Cervera, E  Bosch-Morell, F  Miranda, M  Javier Romero, F 
Citation: Johnsen-Soriano S, etal., Graefes Arch Clin Exp Ophthalmol. 2010 Jul;248(7):985-90. Epub 2010 Mar 6.
Pubmed: (View Article at PubMed) PMID:20213480
DOI: Full-text: DOI:10.1007/s00417-009-1289-x

BACKGROUND: The pathophysiology of the early events leading to diabetic retinopathy is not fully understood. It has been suggested that Inflammatory processes are involved in the development of the disease; however, the concentrations of tissue retinal inflammatory mediators and their possible alteration in diabetic retinopathy have not been described. The aim of this work was to study T-helper cell cytokine and chemokine profiles, and tyrosine nitration in retinal tissue of diabetic rats. METHODS: Cytokines (interleukin IL-1a, IL-1b, IL-2, IL-4, IL-6, IL-10, TNFa, GM-CSF, IFN-g), chemokines (MIP-1a, MIP-2, MIP-3a, MCP-1, GRO/KC, RANTES, Fractalkine), and tyrosine nitration were measured in retinal homogenate obtained from Long-Evans rats after 5 months of experimental diabetes. RESULTS: The T-helper type 1 cytokines IL-2 and INF-gamma, in addition to NO production (measured as nitrotyrosine), were found to be significantly elevated in diabetic rat retina homogenates. None of the other cytokines and chemokines studied were affected by the diabetic condition. CONCLUSIONS: Immunoregulatory cytokines belonging to the Th-1 group (IL-2 and IFN-gamma) were increased in the retina of experimental diabetic rats. Moreover, the nitrotyrosine formation (as an expression of increased NO production) was significantly elevated in the diabetic retina, supporting the concept of an inflammatory element in the development of diabetic retinopathy.

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CRRD Object Information
CRRD ID: 5147915
Created: 2011-08-29
Species: All species
Last Modified: 2011-08-29
Status: ACTIVE



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