You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


ABOUT ARCHIVES
Advanced Search

Welcome   | My Account | E-mail Alerts | Access Rights | Sign In


  Vol. 105 No. 8, August 1987 TABLE OF CONTENTS
  Archives
  •  Online Features
  LABORATORY SCIENCES
 This Article
 •References
 •Full text PDF
 • Reply to article
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citation map
 •Citing articles on HighWire
 •Contact me when this article is cited
 Related Content
 •Similar articles in this journal
 Social Bookmarking
  Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit Add to Technorati Add to Twitter What's this?

Ocular Inflammatory Effects of Intravitreal Interleukin 1

James T. Rosenbaum, MD; John R. Samples, MD; Steven H. Hefeneider, PhD; Edward L. Howes, Jr, MD

Arch Ophthalmol. 1987;105(8):1117-1120.


Abstract

• 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.



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.


Footnotes

Accepted for publication April 22, 1987.

Reprint requests to Oregon Health Sciences University, 3181 SW Sam Jackson Park Rd, L329A, Portland, OR 97201 (Dr Rosenbaum).



Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter     What's this?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Aqueous and Serum Interferon {gamma}, Interleukin (IL) 2, IL-4, and IL-10 in Patients With Uveitis
Lacomba et al.
Arch Ophthalmol 2000;118:768-772.
ABSTRACT | FULL TEXT  

Toxoplasma gondii Infection Induces Gene Expression and Secretion of Interleukin 1 (IL-1), IL-6, Granulocyte-Macrophage Colony-Stimulating Factor, and Intercellular Adhesion Molecule 1 by Human Retinal Pigment Epithelial Cells
Nagineni et al.
Infect. Immun. 2000;68:407-410.
ABSTRACT | FULL TEXT  

IL-1 and TNF Receptor-Deficient Mice Show Decreased Inflammation in an Immune Complex Model of Uveitis
Brito et al.
IOVS 1999;40:2583-2589.
ABSTRACT | FULL TEXT  

The Potential Angiogenic Role of Macrophages in the Formation of Choroidal Neovascular Membranes
Oh et al.
IOVS 1999;40:1891-1898.
ABSTRACT | FULL TEXT  

Activity of an Interleukin 1 Receptor Antagonist in Rabbit Models of Uveitis
Rosenbaum and Boney
Arch Ophthalmol 1992;110:547-549.
ABSTRACT  





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 1987 American Medical Association. All Rights Reserved.