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Infection and Immunity, May 2001, p. 2988-2995, Vol. 69, No. 5
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.5.2988-2995.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Exacerbation of Acanthamoeba Keratitis in Animals Treated with Anti-Macrophage Inflammatory Protein 2 or Antineutrophil Antibodies

Michael Hurt, Sherine Apte, Henry Leher, Kevin Howard, Jerry Niederkorn, and Hassan Alizadeh*

Department of Ophthalmology, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390

Received 10 October 2000/Returned for modification 25 November 2000/Accepted 8 February 2001

Neutrophils are thought to be involved in many infectious diseases and have been found in high numbers in the corneas of patients with Acanthamoeba keratitis. Using a Chinese hamster model of keratitis, conjunctival neutrophil migration was manipulated to determine the importance of neutrophils in this disease. Inhibition of neutrophil recruitment was achieved by subconjunctival injection with an antibody against macrophage inflammatory protein 2 (MIP-2), a powerful chemotactic factor for neutrophils which is secreted by the cornea. In other experiments, neutrophils were depleted by intraperitoneal injection of anti-Chinese hamster neutrophil antibody. The inhibition of neutrophils to the cornea resulted in an earlier onset and more severe infection compared to controls. Anti-MIP-2 antibody treatment produced an almost 35% reduction of myeloperoxidase activity in the cornea 6 days postinfection, while levels of endogenous MIP-2 secretion increased significantly. Recruitment of neutrophils into the cornea via intrastromal injections of recombinant MIP-2 generated an initially intense inflammation that resulted in the rapid resolution of the corneal infection. The profound exacerbation of Acanthamoeba keratitis seen when neutrophil migration was inhibited, combined with the rapid clearing of the disease in the presence of increased neutrophils, strongly suggests that neutrophils play an important role in combating Acanthamoeba infections in the cornea.

* Corresponding author. Mailing address: Department of Ophthalmology, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390. Phone: (214) 648-4732. Fax: (214) 648-9061. E-mail: Hassan.Alizadeh{at}UTSouthwestern.edu.

Infection and Immunity, May 2001, p. 2988-2995, Vol. 69, No. 5
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.5.2988-2995.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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