title: The effect of infliximab, cyclosporine A and recombinant IL-10 on vitreous cytokine levels in experimental autoimmune uveitis.
abstract: BACKGROUND
  To identify the effect of infliximab, cyclosporine A and recombinant IL-10 in experimental autoimmune uveitis.
  
  
  METHODS
  Sixty male rats were assigned to five groups of 12 each. All the groups (except the control group) were administered 30 microg retinal-S antigen intraperitoneally. On the 14th day, after confirmation of uveitis with histopathological study, daily cyclosporine A injection was given in cyclosporine A treatment group and physiological serum in the uveitis-induced placebo treatment and control groups. In the infliximab treatment group, infliximab was administered on the 14th, 15th, 17th, 19th and 21st days. In the recombinant IL-10 treatment group, three doses of recombinant IL-10 were given four hours and a half hours before and eight hours after retinal-S antigen administration. On the 21st day of the study, all rats were sacrificed and vitreous cytokine levels (IL-1, IL-6, IL-8 and TNF-alpha) were studied with ELISA.
  
  
  RESULTS
  In the treatment groups, cytokine levels (IL-1, IL-6 and TNF-alpha) were significantly lower than the uveitis-induced placebo treatment group. Compared with the control group, there was no significant difference with respect to TNF-alpha and IL-8 in the infliximab treatment group; IL-8 in the cyclosporine A treatment group; IL-6 and IL-8 in the recombinant IL-10 treatment group. The drugs used did not significantly differ in respect to their effects on vitreous IL-6, IL-8 and TNF-alpha levels.
  
  
  CONCLUSIONS
  Cyclosporine A, infliximab and recombinant IL-10 reduce the vitreous cytokines levels. Among these drugs, recombinant IL-10, which is still in its experimental phase, might be considered as a new therapeutic agent.
authors.affiliation: Firat University School of Medicine, Department of Ophthalmology, Elazig, Turkey.
authors.forename: Tamer
authors.initials: T
authors.lastname: Demir
authors.forename: Ahmet
authors.initials: A
authors.lastname: Gödekmerdan
authors.forename: Mehmet
authors.initials: M
authors.lastname: Balbaba
authors.forename: Peykan
authors.initials: P
authors.lastname: Türkçüoglu
authors.forename: Fulya
authors.initials: F
authors.lastname: Ilhan
authors.forename: Nesrin
authors.initials: N
authors.lastname: Demir
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000627:therapeutic use; D000911:Antibodies, Monoclonal / Q000008:administration & dosage / Q000627:therapeutic use*; D019393:Arrestin / Q000633:toxicity; D001327:Autoimmune Diseases / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D016572:Cyclosporine / Q000008:administration & dosage / Q000627:therapeutic use*; D016207:Cytokines / Q000378:metabolism*; D004195:Disease Models, Animal; D005500:Follow-Up Studies; D007166:Immunosuppressive Agents / Q000008:administration & dosage / Q000627:therapeutic use; D000069285:Infliximab; D007274:Injections, Intraperitoneal; D016753:Interleukin-10 / Q000008:administration & dosage / Q000627:therapeutic use*; D008297:Male; D051381:Rats; D011917:Rats, Inbred Lew; D011994:Recombinant Proteins; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha; D014605:Uveitis / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism; D014822:Vitreous Body / Q000187:drug effects / Q000378:metabolism*
chemical_list: D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D019393:Arrestin; D015415:Biomarkers; D016207:Cytokines; D007166:Immunosuppressive Agents; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D016572:Cyclosporine; D000069285:Infliximab