αB-Crystallin Protects Retinal Tissue during Staphylococcus aureus - Induced Endophthalmitis

Author:

Whiston Emily A.1,Sugi Norito1,Kamradt Merideth C.2,Sack Coralynn1,Heimer Susan R.1,Engelbert Michael3,Wawrousek Eric F.4,Gilmore Michael S.1,Ksander Bruce R.1,Gregory Meredith S.1

Affiliation:

1. The Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, 20 Staniford Street, Boston, Massachusetts 02114

2. School of Arts and Sciences, Bridgewater State College, 24 Park Avenue, Bridgewater, Massachusetts 02325

3. Edward S. Harkness Eye Institute, Columbia University College of Physicians and Surgeons, 635 West 165th Street, New York, New York

4. National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892

Abstract

ABSTRACT 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 αB-crystallin is upregulated in the retina and prevents apoptosis during immune clearance of the bacteria. In the absence of αB-crystallin, mice display increased retinal apoptosis and retinal damage. We found that S. aureus produces a protease capable of cleaving αB-crystallin to a form that coincides with increased retinal apoptosis and tissue destruction. We conclude that αB-crystallin is important in protecting sensitive retinal tissue during destructive inflammation that occurs during bacterial endophthalmitis.

Publisher

American Society for Microbiology

Subject

Infectious Diseases,Immunology,Microbiology,Parasitology

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