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August 1987

Ocular Inflammatory Effects of Intravitreal Interleukin 1

Author Affiliations

From the Oregon Health Sciences University, Portland (Drs Rosenbaum and Samples); Veterans Administration Medical Center, Portland, Ore (Dr Hefeneider); and San Francisco General Hospital (Dr Howes). Dr Rosenbaum is the recipient of the Dolly Green Award from Research to Prevent Blindness Inc, New York.

Arch Ophthalmol. 1987;105(8):1117-1120. doi:10.1001/archopht.1987.01060080119040

• Locally injected endotoxin induces potent inflammatory changes in the rabbit eye. To clarify the possible role of interleukin 1 (II-1), an endotoxin-induced monokine, in rabbit eye inflammation, we injected rabbits with recombinant 11-1 (rII-1). Twelve and a half to 200 U of intravit really injected rII-1 consistently induced inflammation, which was documented using slit-lamp biomicroscopy, histologic methods, or direct quantitation of protein in the aqueous humor. Responses including a cellular infiltrate in the anterior chamber, protein extravasation, and iris vessel dilatation became evident within six hours, peaked at 24 hours, and began to recede by 48 to 72 hours after the injection. Pathologic changes primarily occurred in the anterior chamber and included edema, hemorrhage, and cellular infiltration. Locally injected corticosteroid reduced but did not prevent rII-1-induced changes in vascular permeability. Heat-inactivated rII-1 induced minimal changes, as determined by histologic methods, slit-lamp examination, or direct protein measurement. These data support the conclusion that 11-1 should be considered as a potential mediator of ocular inflammation.