Whiston, E. A.Sugi, N.Kamradt, M. C.Sack, C.Heimer, S. R.Engelbert, M.Wawrousek, E. F.Gilmore, MichaelKsander, BruceGregory, M. S.2018-03-272008Whiston, E. A., N. Sugi, M. C. Kamradt, C. Sack, S. R. Heimer, M. Engelbert, E. F. Wawrousek, M. S. Gilmore, B. R. Ksander, and M. S. Gregory. 2008. B-Crystallin Protects Retinal Tissue During Staphylococcus Aureus- Induced Endophthalmitis. Infection and Immunity 76, no. 4: 1781–1790. doi:10.1128/iai.01285-07.0019-9567http://nrs.harvard.edu/urn-3:HUL.InstRepos:35141057Bacterial 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.en-US B-Crystallin Protects Retinal Tissue during Staphylococcus aureus- Induced EndophthalmitisJournal Article2018-03-2710.1128/IAI.01285-07