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Infection and Immunity, April 2008, p. 1781-1790, Vol. 76, No. 4
0019-9567/08/$08.00+0     doi:10.1128/IAI.01285-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

{alpha}B-Crystallin Protects Retinal Tissue during Staphylococcus aureus- Induced Endophthalmitis{triangledown}

Emily A. Whiston,1,{dagger} Norito Sugi,1,{dagger} Merideth C. Kamradt,2 Coralynn Sack,1 Susan R. Heimer,1 Michael Engelbert,3 Eric F. Wawrousek,4 Michael S. Gilmore,1 Bruce R. Ksander,1 and Meredith S. Gregory1*

The Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, 20 Staniford Street, Boston, Massachusetts 02114,1 School of Arts and Sciences, Bridgewater State College, 24 Park Avenue, Bridgewater, Massachusetts 02325,2 Edward S. Harkness Eye Institute, Columbia University College of Physicians and Surgeons, 635 West 165th Street, New York, New York,3 National Eye Institute, National Institutes of Health, Bethesda, Maryland 208924

Received 20 September 2007/ Returned for modification 19 October 2007/ Accepted 22 January 2008

Bacterial infections of the eye highlight a dilemma that is central to all immune-privileged sites. On the one hand, immune privilege limits inflammation to prevent bystander destruction of normal tissue and loss of vision. On the other hand, bacterial infections require a robust inflammatory response for rapid clearance of the pathogen. We demonstrate that the retina handles this dilemma, in part, by activation of a protective heat shock protein. During Staphylococcus aureus-induced endophthalmitis, the small heat shock protein {alpha}B-crystallin is upregulated in the retina and prevents apoptosis during immune clearance of the bacteria. In the absence of {alpha}B-crystallin, mice display increased retinal apoptosis and retinal damage. We found that S. aureus produces a protease capable of cleaving {alpha}B-crystallin to a form that coincides with increased retinal apoptosis and tissue destruction. We conclude that {alpha}B-crystallin is important in protecting sensitive retinal tissue during destructive inflammation that occurs during bacterial endophthalmitis.

* Corresponding author. Mailing address: Schepens Eye Research Institute, 20 Staniford Street, Boston, MA 02114. Phone: (617) 912-7455. Fax: (617) 912-0113. E-mail: meredith.gregory{at}schepens.harvard.edu

{triangledown} Published ahead of print on 28 January 2008.

Editor: A. J. Bäumler

{dagger} E.A.W. and N.S. contributed equally to this work.

Infection and Immunity, April 2008, p. 1781-1790, Vol. 76, No. 4
0019-9567/08/$08.00+0     doi:10.1128/IAI.01285-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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