title: [Preventive effect of anterior chamber associated immune deviation on endotoxin-induced uveitis].
abstract: OBJECTIVE
  To determine the effect of anterior chamber associated immune deviation (ACAID) on endotoxin-induced uveitis (EIU) and the possible mechanism.
  
  
  METHODS
  ACAID animal model was induced by injection of 5 microl IRBP (10 microg/microl) into the anterior chamber (AC) of Spar-Dawley (SD) rats. Then 200 microg LPS was injected into hind footpads at different time points after AC inoculation. The animals were randomly divided into 3 groups: positive control (LPS injection only), 3 d group (LPS injection 3 days after IRBP inoculation), 7 d group (LPS injection 7 days after IRBP inoculation). Delayed type hypersensitivity (DTH) was examined to determine the development of ACAID. Then the serum level of IL-10 was evaluated by ELISA, and GATA-3 expression at the different time points after IRBP injection was assayed by reverse transcription polymerase chain reaction (RT-PCR) and Western blot on mRNA and protein level respectively. The ocular inflammation was observed clinically; at the same time, the eye was extirpated and histological examination was performed.
  
  
  RESULTS
  In control and 3 d groups, significant DTH reaction was induced, but the serum level of IL-10 could not be detected and GATA-3 expression was not increased. While in 7 d group, the DTH reaction could not be induced, and IL-10 and GATA-3 expression increased significantly at both the mRNA and protein levels. The clinical manifestation was significantly alleviated in the 7 d group; Histological examination displayed that the inflammatory cells were significantly reduced in iris/ciliary body, anterior and posterior chambers, vitreous body and retina of the rats in 7 d group.
  
  
  CONCLUSIONS
  The development of ACAID can reduce the ocular inflammation induced by LPS, that is related to the increase of GATA-3 and IL-10 expression.
authors.affiliation: Beijing Tongren Eye Center, Tongren Hospital, Capital University of Medical Science, Beijing 100730, China.
authors.forename: Tao
authors.initials: T
authors.lastname: Fu
authors.forename: Pei-Zeng
authors.initials: PZ
authors.lastname: Yang
authors.forename: Xiang-Kun
authors.initials: XK
authors.lastname: Huang
authors.forename: Hong-Yan
authors.initials: HY
authors.lastname: Zhou
authors.forename: Fen-Fang
authors.initials: FF
authors.lastname: Li
authors.forename: Qiang
authors.initials: Q
authors.lastname: Huang
mesh_terms: D000818:Animals; D000867:Anterior Chamber / Q000276:immunology*; D001082:Aqueous Humor / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D004731:Endotoxins; D005136:Eye Proteins / Q000276:immunology*; D050990:GATA3 Transcription Factor; D006968:Hypersensitivity, Delayed / Q000276:immunology; D016753:Interleukin-10 / Q000097:blood; D008297:Male; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012177:Retinol-Binding Proteins / Q000276:immunology*; D015534:Trans-Activators / Q000096:biosynthesis / Q000235:genetics; D014605:Uveitis / Q000139:chemically induced / Q000276:immunology*; D000099214:Retinol-Binding Proteins, Interstitial
chemical_list: D004268:DNA-Binding Proteins; D004731:Endotoxins; D005136:Eye Proteins; D050990:GATA3 Transcription Factor; D016753:Interleukin-10; D012333:RNA, Messenger; D012177:Retinol-Binding Proteins; D015534:Trans-Activators; D000099214:Retinol-Binding Proteins, Interstitial