March 1998
Volume 39, Issue 3
Free
Articles  |   March 1998
Mice deficient in tumor necrosis factor receptors p55 and p75, interleukin-4, or inducible nitric oxide synthase are susceptible to endotoxin-induced uveitis.
Author Affiliations
  • J R Smith
    Department of Ophthalmology, Flinders University of South Australia, Bedford Park, Australia.
  • P H Hart
    Department of Ophthalmology, Flinders University of South Australia, Bedford Park, Australia.
  • D J Coster
    Department of Ophthalmology, Flinders University of South Australia, Bedford Park, Australia.
  • K A Williams
    Department of Ophthalmology, Flinders University of South Australia, Bedford Park, Australia.
Investigative Ophthalmology & Visual Science March 1998, Vol.39, 658-661. doi:
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    • Get Citation

      J R Smith, P H Hart, D J Coster, K A Williams; Mice deficient in tumor necrosis factor receptors p55 and p75, interleukin-4, or inducible nitric oxide synthase are susceptible to endotoxin-induced uveitis.. Invest. Ophthalmol. Vis. Sci. 1998;39(3):658-661.

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Abstract

PURPOSE: To investigate the roles of tumor necrosis factor-alpha (TNF-alpha), interleukin-4 (IL-4), and inducible nitric oxide synthase (iNOS) in endotoxin-induced uveitis (EIU) using gene knock-out mice. METHODS: Mice (C57BL/6 x 129) either of normal phenotype or deficient in the genes encoding one or both tumor necrosis factor receptors (TNFR p55 and TNFR p75), IL-4, or iNOS were given footpad injections of 400 micrograms Escherichia coli lipopolysaccharide. Animals were killed 24 hours later, and infiltrating cells were counted on 5-micron ocular cross-sections through the optic nerve. RESULTS: All abnormal mouse phenotypes were susceptible to EIU. Yet, TNFR p55 and IL-4 gene knock-out mice experienced less ocular inflammation than control animals (P = 0.021 and 0.007, respectively), whereas disease was not reduced for iNOS-deficient mice. Mice deficient in TNFR p55 and TNFR p75 experienced milder EIU than mice lacking TNFR p75 alone (P = 0.046). CONCLUSIONS: Mice deficient in TNFR p55 and TNFR p75, IL-4, or iNOS retain the susceptibility to EIU, but TNF-alpha and IL-4 influence the influx of inflammatory cells to the eye during this disease.

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