|Title:||行政院國家科學委員會專題研究計畫期中進度報告:細胞間素活化轉錄因子 NF-KB 引起眼球內炎性反應的研究（2/3）||Authors:||楊長豪||Issue Date:||2000||Publisher:||臺北市：國立臺灣大學醫學院眼科||Abstract:||
Purpose. To demonstrate the expression and location of fractalkine and receptor,
CX3CR1, in iris/ciliary body and thus establish their roles in experimental
autoimmune anterior uveitis, an animal model of human acute anterior uveitis.
Methods. Uveitis was induced with the injection of melanin-associated antigen
intraperitoneally and into the left footpad simultaneously. Some rats were treated with
a putative NF-κB inhibitor, pyrrolidine dithiocarbamate (PDTC; 40 mg/kg/day) every
day after immunization. At defined time points, fractalkine and CX3CR1 mRNA
expression were semiquantified by using RT-PCR. Fractalkine in aqueous humor was
determined by ELISA. The cellular sources of fractalkine were determined by
Results. Fractalkine mRNA was found to be upregulated in iris/ciliary body 9 days
after immunization, preceding clinical disease onset. CX3CR1 mRNA exhibited peak
levels at day 14, coincident with disease onset. Fractalkine in aqueous humor showed
a similar expression profile to mRNA expression. PDTC markedly inhibited the
expression of fractalkine mRNA in iris/ciliary body and fractalkine protein in aqueous
humor. Immuhistochemical staining revealed fractalkine was prominently expressed
on vascular endothelial cells.
Conclusions. This study was the first to provide evidences of fractalkine –CX3CR1
interactions in the genesis of experimental autoimmune anterior uveitis. The
activation of fractalkine gene is, at least in part, via a NF-κB-dependent pathway.
Therefore, selective anti-fractalkine or anti- NF-κB therapy may become a therapeutic
potential for acute anterior uveitis treatment.
|Appears in Collections:||醫學系|
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