Human immunoglobulin preparations for intravenous use prevent endotoxin-induced uveitis in rats

Citation
E. Obrador et al., Human immunoglobulin preparations for intravenous use prevent endotoxin-induced uveitis in rats, OPHTHAL RES, 31(1), 1999, pp. 59-67
Citations number
36
Categorie Soggetti
da verificare
Journal title
OPHTHALMIC RESEARCH
ISSN journal
00303747 → ACNP
Volume
31
Issue
1
Year of publication
1999
Pages
59 - 67
Database
ISI
SICI code
0030-3747(199901/02)31:1<59:HIPFIU>2.0.ZU;2-8
Abstract
Objective: We analyzed the preventive effect of immunoglobulins for intrave nous use (IVIgs) in endotoxin-induced uveitis (EIU), a disease related to t umor necrosis factor a (TNF-alpha) production. Materials and Methods: EIU w as the experimental model in Lewis rats, injecting a systemic dose of 150 m u g of lipopolysaccharide (LPS) into the rat's footpad. Half of them were t reated with 5 serial intravenous doses of 100 mg of IVIg during the 5 days prior to LPS injection. Eyes were repeatedly examined with a slitlamp, rats were killed and their eyes enucleated for histopathologic study at the 2nd , 16th and 24th hours. TNF-alpha serum revels were measured in aqueous humo r at several time intervals by a bioassay using L-929 mouse fibroblasts. Aq ueous humor proteins were detected by the Bradford method. Results: IVIg tr eatment prevented EIU development, treated animals showing a lower grade of ocular inflammation beyond the 2nd hour (Fisher test, p > 0.05). Inflammat ory cell infiltration was significantly reduced in the iris, ciliary body a nd anterior chamber at a 24-hour interval (Wilcoxon test, p < 0.05). This p rotection was associated with lower levels of TNF-alpha in serum at all tim e intervals and in aqueous humor at 16 h (Student's t test, p < 0.05), whil e differences were not significant between the samples of aqueous humor col lected at 2 h. Protein exudate was not reduced in the treated group. Conclu sions: Repeated IVIg injections could be useful in the preventive treatment of EIU probably mediated by a decrease in TNF-alpha release.