October 1991
Volume 32, Issue 11
Free
Articles  |   October 1991
Effect of interferon on a primary conjunctival epithelial cell model of trachoma.
Author Affiliations
  • P A Rapoza
    Department of Ophthalmology, University of Wisconsin, Madison 53705.
  • S G Tahija
    Department of Ophthalmology, University of Wisconsin, Madison 53705.
  • J P Carlin
    Department of Ophthalmology, University of Wisconsin, Madison 53705.
  • S L Miller
    Department of Ophthalmology, University of Wisconsin, Madison 53705.
  • M L Padilla
    Department of Ophthalmology, University of Wisconsin, Madison 53705.
  • G I Byrne
    Department of Ophthalmology, University of Wisconsin, Madison 53705.
Investigative Ophthalmology & Visual Science October 1991, Vol.32, 2919-2923. doi:https://doi.org/
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      P A Rapoza, S G Tahija, J P Carlin, S L Miller, M L Padilla, G I Byrne; Effect of interferon on a primary conjunctival epithelial cell model of trachoma.. Invest. Ophthalmol. Vis. Sci. 1991;32(11):2919-2923. doi: https://doi.org/.

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

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Abstract

An in vitro human primary conjunctival epithelial system was adapted to determine if the effects of interferon-gamma (IFN-gamma), as described in cultured cell lines, were applicable to human ocular infection with Chlamydia trachomatis, Primary human epithelial cell cultures were exposed to varying concentrations of IFN-gamma. The treatment resulted in the induction of the tryptophan decyclizing enzyme indolamine 2,3-deoxygenase (IDO) in a dose-dependent manner as determined by assaying the conversion of tryptophan to its metabolites using reversed-phase high-performance liquid chromatography. Little IDO induction occurred in the presence of IFN-alpha or IFN-beta. Catabolism of up to 38% of available tryptophan occurred in IFN-gamma-treated cells in contrast to controls that showed only baseline activity. Cells cultured with IFN-gamma and then infected with an ocular isolate of C. trachomatis (TW-5), had a reduction in the percentage of inclusion-containing cells by over 80% in a dose-dependent manner. Reversal by the addition of exogenous tryptophan substantiated that IFN-gamma-mediated induction of IDO and catabolism of tryptophan were responsible for inhibition of intracellular growth of C. trachomatis.

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