title: IL-2 and IFN-gamma in the retina of diabetic rats.
abstract: 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.
authors.affiliation: Fundación Oftalmológica del Mediterráneo, Bifurcación Pio Baroja-General Avilés, s/n 46015, Valencia, Spain.
authors.forename: Siv
authors.initials: S
authors.lastname: Johnsen-Soriano
authors.forename: María
authors.initials: M
authors.lastname: Sancho-Tello
authors.forename: Emma
authors.initials: E
authors.lastname: Arnal
authors.forename: Amparo
authors.initials: A
authors.lastname: Navea
authors.forename: Enrique
authors.initials: E
authors.lastname: Cervera
authors.forename: Francisco
authors.initials: F
authors.lastname: Bosch-Morell
authors.forename: Maria
authors.initials: M
authors.lastname: Miranda
authors.forename: Francisco
authors.initials: F
authors.lastname: Javier Romero
mesh_terms: D000818:Animals; D002386:Cataract / Q000276:immunology / Q000378:metabolism; D018925:Chemokines / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000276:immunology / Q000378:metabolism; D003930:Diabetic Retinopathy / Q000276:immunology* / Q000378:metabolism*; D004195:Disease Models, Animal; D007371:Interferon-gamma / Q000378:metabolism*; D016753:Interleukin-10 / Q000378:metabolism; D053582:Interleukin-1alpha / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D007376:Interleukin-2 / Q000378:metabolism*; D015847:Interleukin-4 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism; D051381:Rats; D020318:Rats, Long-Evans; D012160:Retina / Q000276:immunology / Q000378:metabolism*; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014443:Tyrosine / Q000031:analogs & derivatives / Q000378:metabolism
chemical_list: D018925:Chemokines; D053582:Interleukin-1alpha; D053583:Interleukin-1beta; D007376:Interleukin-2; D015850:Interleukin-6; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D015847:Interleukin-4; D009569:Nitric Oxide; C002744:3-nitrotyrosine; D014443:Tyrosine; D007371:Interferon-gamma