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αB-Crystallin Protects Retinal Tissue during Staphylococcus aureus - Induced Endophthalmitis
Author(s) -
Emily Whiston,
N. Sugi,
Merideth C. Kamradt,
Coralynn Sack,
Susan R. Heimer,
Michael Engelbert,
Eric F. Wawrousek,
Michael S. Gilmore,
Bruce R. Ksander,
Meredith S. Gregory
Publication year - 2008
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.01285-07
Subject(s) - immune privilege , biology , staphylococcus aureus , endophthalmitis , retina , inflammation , immune system , heat shock protein , microbiology and biotechnology , retinal , immunology , staphylococcal infections , bacteria , biochemistry , genetics , neuroscience , gene
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 alphaB-crystallin is upregulated in the retina and prevents apoptosis during immune clearance of the bacteria. In the absence of alphaB-crystallin, mice display increased retinal apoptosis and retinal damage. We found that S. aureus produces a protease capable of cleaving alphaB-crystallin to a form that coincides with increased retinal apoptosis and tissue destruction. We conclude that alphaB-crystallin is important in protecting sensitive retinal tissue during destructive inflammation that occurs during bacterial endophthalmitis.

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