| First Author | Smith JR | Year | 1998 |
| Journal | Invest Ophthalmol Vis Sci | Volume | 39 |
| Issue | 3 | Pages | 658-61 |
| PubMed ID | 9501881 | Mgi Jnum | J:46231 |
| Mgi Id | MGI:1197389 | Citation | Smith JR, et al. (1998) 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 39(3):658-61 |
| abstractText | 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. |
