April 1991
Volume 32, Issue 5
Free
Articles  |   April 1991
Ocular inflammation stimulated by intravitreal interleukin-8 and interleukin-1.
Author Affiliations
  • M R Ferrick
    Howard Hughes Medical Institute, National Eye Institute, Bethesda, MD 20892.
  • S R Thurau
    Howard Hughes Medical Institute, National Eye Institute, Bethesda, MD 20892.
  • M H Oppenheim
    Howard Hughes Medical Institute, National Eye Institute, Bethesda, MD 20892.
  • C P Herbort
    Howard Hughes Medical Institute, National Eye Institute, Bethesda, MD 20892.
  • M Ni
    Howard Hughes Medical Institute, National Eye Institute, Bethesda, MD 20892.
  • C O Zachariae
    Howard Hughes Medical Institute, National Eye Institute, Bethesda, MD 20892.
  • K Matsushima
    Howard Hughes Medical Institute, National Eye Institute, Bethesda, MD 20892.
  • C C Chan
    Howard Hughes Medical Institute, National Eye Institute, Bethesda, MD 20892.
Investigative Ophthalmology & Visual Science April 1991, Vol.32, 1534-1539. doi:
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      M R Ferrick, S R Thurau, M H Oppenheim, C P Herbort, M Ni, C O Zachariae, K Matsushima, C C Chan; Ocular inflammation stimulated by intravitreal interleukin-8 and interleukin-1.. Invest. Ophthalmol. Vis. Sci. 1991;32(5):1534-1539.

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

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Abstract

Interleukin-8 (IL-8), a cytokine with neutrophil chemotactic and activating properties, is known to be stimulated by IL-1. Fischer rats are more resistant to inflammation than Lewis rats probably due to a higher corticosteroid stress response. To determine the role of IL-8 in ocular inflammation, the effect of intravitreal injection of IL-8 was compared with that of IL-1 in both Lewis and Fischer rats. The IL-8, IL-1 alpha, or sterile balanced salt solution (control) was injected into one eye of each animal. Both IL-8 and IL-1 alpha caused inflammation in the eye of both strains, as detected by leukocyte counts of the anterior chamber and histopathologic examination. The eyes of animals injected with a cytokine had significantly higher numbers of leukocytes compared with eyes of control animals. Histopathologic examination confirmed these findings. The IL-1 alpha induced inflammation more consistently and more severely than the most effective dose of IL-8. This finding agreed with the concept of IL-1 initiating a cascade of inflammatory mediators including IL-8, which acts more specifically on a smaller population of leukocytes. A contralateral response was observed in the uninjected eye of experimental and control animals. The contralateral response in animals receiving the cytokines was significantly greater than that in controls. Lewis rats show a higher inflammatory response to the injections than do the Fischer rats. These data suggest that IL-8 may be active as one component in neutrophil-mediated ocular inflammation.

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