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Originally published In Press as doi:10.1167/iovs.08-2085 on June 27, 2008
 (Investigative Ophthalmology and Visual Science. 2008;49:4482-4489.)
© 2008 by The Association for Research in Vision and Ophthalmology, Inc.
DOI:  10.1167/iovs.08-2085
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A Role for Tumor Necrosis Factor-{alpha} in Experimental Bacillus cereus Endophthalmitis Pathogenesis

Raniyah T. Ramadan,1 Andrea L. Moyer,2 and Michelle C. Callegan1,2,3,4

1From the Oklahoma Center for Neuroscience and the 2Departments of Microbiology and Immunology and 3Ophthalmology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; and the 4Molecular Pathogenesis of Eye Infections Research Center, Dean A. McGee Eye Institute, Oklahoma City, Oklahoma.

PURPOSE. To determine the contribution of tumor necrosis factor-alpha (TNF{alpha}) in the pathogenesis of experimental Bacillus cereus endophthalmitis.

METHODS. Experimental B. cereus endophthalmitis was induced in wild-type control (B6.129F1) and age-matched homozygous TNF{alpha} knockout mice (TNF{alpha}–/–, B6.129S6-Tnftm1Gk1/J). At various times after infection, eyes were analyzed by electroretinography and were harvested for quantitation of bacteria, myeloperoxidase, proinflammatory cytokines and chemokines, and histologic analysis.

RESULTS. B. cereus replicated more rapidly in the eyes of TNF{alpha}–/– mice than in the eyes of B6.129F1 mice. Retinal function decreased more rapidly in TNF{alpha}–/– mice than in B6.129F1 mice. Retinal layers were not as structurally intact at 6 and 12 hours after infection in TNF{alpha}–/– eyes as in B6.129F1 eyes. Histologic analysis suggested less polymorphonuclear leukocyte (PMN) infiltration into the vitreous of TNF{alpha}–/– mice than of B6.129F1 mice. B6.129F1 eyes also had greater myeloperoxidase concentrations than did eyes of TNF{alpha}–/– mice. In general, concentrations of proinflammatory cytokines and chemokines (IL-1β, KC, IL-6, and MIP-1{alpha}) were greater in eyes of TNF{alpha}–/– mice than of B6.129F1 mice.

CONCLUSIONS. TNF{alpha} is important to intraocular pathogen containment by PMNs during experimental B. cereus endophthalmitis. In the absence of TNF{alpha}, fewer PMNs migrated into the eye, facilitating faster bacterial replication and retinal function loss. Although greater concentrations of proinflammatory cytokines were synthesized in the absence of TNF{alpha}, the resultant inflammation was diminished, and an equally devastating course of infection occurred.






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