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Investigative Ophthalmology & Visual Science, Vol 38, 257-260, Copyright © 1997 by Association for Research in Vision and Ophthalmology
ARTICLES AND REPORTS |
B Peng, Q Li, FG Roberge and CC Chan
Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892-1858, USA.
PURPOSE: Transforming growth factor beta-1 (TGF beta-1) can modulate inflammation. Endotoxin-induced uveitis (EIU) is characterized by acute ocular inflammation related to the release of cytokines, including interleukin (IL)-6. The authors investigated the effect of TGF beta-1 on EIU in mice. METHODS: Three independent experiments were performed. Endotoxin-induced uveitis was induced in C3H/HeN mice by an injection of 200 micrograms of lipopolysaccharide (LPS). Two micrograms of TGF beta-1 in 0.1 ml phosphate-buffered saline (PBS) or 0.1 ml PBS alone was administered intraperitoneally at 8 hours after LPS injection. Twenty-four hours after LPS injection, the aqueous humor of the right eyes was collected for leukocyte count, protein concentration, and IL-6 assay. Left eyes were processed for routine histology. RESULTS: TGF beta-1-treated mice showed less ocular inflammation histologically than to the animals that were given PBS. This was confirmed by decreases in leukocyte count, protein concentration, and IL-6 level in the aqueous humor. CONCLUSIONS: TGF beta-1 inhibits the development of EIU. TGF beta-1 may be useful for the modulation of uveitis in humans.
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