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Olivier Marie, Brigitte Thillaye-Goldenberg, Marie-Christine Naud, Yvonne de Kozak; Inhibition of Endotoxin-Induced Uveitis and Potentiation of Local TNF-α and Interleukin-6 mRNA Expression by Interleukin-13. Invest. Ophthalmol. Vis. Sci. 1999;40(10):2275-2282.
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purpose. To investigate the effect of systemic injections of interleukin (IL)-13
on the development of endotoxin-induced uveitis (EIU) in the rat.
methods. EIU was induced in Lewis rats by a single footpad injection of
lipopolysaccharide (LPS; 350 μg/kg) from Salmonella typhimurium.
Rats were treated with a subcutaneous injection in the back of
recombinant human IL-13 (50 μg/kg in 0.2 ml of saline) performed 30
minutes before LPS injection and 6 and 10 hours afterward. At 23 hours
after LPS injection, EIU was evaluated by slit-lamp examination and by
counts of inflammatory cells on cryostat sections after specific
immunostaining. The expression of nitric oxide synthase (NOS)–II in
ocular tissues was determined by dual immunofluorescent staining and
the release of nitrite in aqueous humor by Griess reaction. Cytokine
gene expression in the iris/ciliary body, choroid, and retina was
evaluated by reverse transcription–polymerase chain reaction.
results. At 24 hours after LPS injection, significant clinical inhibition of
ocular inflammation and fibrin deposition in the eye was observed in
IL-13–treated rats. Quantitative analysis of ocular tissues revealed a
significant decrease of OX-42+ cells (microglia, activated macrophages,
dendritic cells, and polymorphonuclear leukocytes) and ED-1+ cells
(monocytes/macrophages and dendritic cells). No effect on ED2+ cells
(resident tissue macrophages) was found. Treatment with IL-13 decreased
nitrite levels in aqueous humor and enhanced the expression of tumor
necrosis factor-α (TNF-α) and IL-6 mRNA in ocular tissues.
conclusions. Interleukin-13 treatment inhibits LPS-induced ocular inflammation with
inhibition of nitrite release and increased TNF and IL-6 production in
the eye. These results confirm the role of the NO pathway in the
pathogenesis of EIU and suggest the involvement of TNF and IL-6 in the
downregulation of ocular inflammation.
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