May 2007
Volume 48, Issue 13
ARVO Annual Meeting Abstract  |   May 2007
The Contribution of TNF-Alpha to Bacillus cereus Endophthalmitis Pathogenesis
Author Affiliations & Notes
  • R. Ramadan
    Univ of Oklahoma Hlth Sci Ctr, Oklahoma City, Oklahoma
    Oklahoma Center for Neuroscience,
  • A. L. Moyer
    Univ of Oklahoma Hlth Sci Ctr, Oklahoma City, Oklahoma
    Microbiology and Immunology,
  • M. C. Callegan
    Univ of Oklahoma Hlth Sci Ctr, Oklahoma City, Oklahoma
    Molecular Pathogenesis of Eye Infections Research Center, Dean McGee Eye Institute, Oklahoma City, Oklahoma
  • Footnotes
    Commercial Relationships R. Ramadan, None; A.L. Moyer, None; M.C. Callegan, None.
  • Footnotes
    Support NIH grant R01EY12985 and Lew R. Wasserman Award from Research to Prevent Blindness, Inc. (to MCC) and an NIH CORE grant P30 EY12191 (to R.E. Anderson)
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 2663. doi:
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    • Get Citation

      R. Ramadan, A. L. Moyer, M. C. Callegan; The Contribution of TNF-Alpha to Bacillus cereus Endophthalmitis Pathogenesis. Invest. Ophthalmol. Vis. Sci. 2007;48(13):2663.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose:: To elucidate the contribution of TNF alpha production to inflammation and retinal function loss during experimental Bacillus endophthalmitis.

Methods:: Experimental Bacillus endophthalmitis was induced in wild type (B6.129S6) or TNF-alpha knockout mice (B6.129S6-Tnftm1Gk1). At various times postinfection, eyes were analyzed by electroretinography, and harvested for bacterial quantitation, myeloperoxidase and proinflammatory cytokine activities, and histological analysis.

Results:: Retinal function decreased less rapidly in the TNF-alpha deficient mice than wild-type control mice. Histological analysis suggested less PMN infiltration in the vitreous in TNF-alpha knockout mice than in wild type control mice, an observation that correlated with decreased myeloperoxidase activities in eyes of TNF-alpha deficient mice. Structural integrity of retinal layers was also less disrupted at 6 and 12 hours postinfection in TNF-alpha deficient mice as compared to wild-type controls. Proinflammatory cytokine levels were greater in TNF-alpha deficient mice than in wild-type controls. IL-1beta, KC (IL-8), IL-6, and MIP1alpha increase significantly up to 12 hours post-infection during Bacillus endophthalmitis.

Conclusions:: TNF-alpha appears to contribute significantly to the evolving pathogenesis of experimental Bacillus endophthalmitis. Additional immune mediators may compensate for TNF-alpha in its absence, resulting in a slower course of infection. Future studies are focused on the roles of these mediators in the pathogenesis of Bacillus endophthalmitis.

Keywords: bacterial disease • endophthalmitis • cytokines/chemokines 

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