Abstract
Experimental coronavirus retinopathy (ECOR) is a virally triggered model of retinal degeneration composed of both genetic and autoimmune components. Since TNF-α plays a role in immune-mediated processes we evaluated the levels of TNF-α/TNF-α receptors and the downstream signaling molecule nitric oxide (NO) during disease in both retinal degeneration susceptible BALB/c and degeneration resistant CD-1 mice. Following coronavirus injection, TNF-α mRNA was detected at higher levels within the retinas, and concentrations of TNF-α (p < 0.005) and sTNFR1 (p < 0.0005) proteins were increased within the sera of BALB/c but not CD-1 mice. While concentrations of sTNFR2 proteins were elevated in both BALB/c (p < 0.00005) and CD-1 (p < 0.005) mice compared to controls, concentrations were higher in BALB/c mice (p < 0.0005). Gene expression of iNOS while initially high in BALB/c mice decreased during the acute phase of infection, while it increased in CD-1 mice. These trends are attributable to differences in monocyte TNFR2 release (p < 0.0005) between the strains since sTNFR2 decreased (p < 0.01) levels of NO production. These studies demonstrate that retinal degeneration following viral infection is associated with increased release of TNF-α/TNF receptors combined with a down-regulation of NO. Furthermore they suggest that these molecules are involved in alterations in immune response leading to autoimmune reactivity.
Original language | English (US) |
---|---|
Pages (from-to) | 65-74 |
Number of pages | 10 |
Journal | Journal of Neuroimmunology |
Volume | 166 |
Issue number | 1-2 |
DOIs | |
State | Published - Sep 2005 |
Keywords
- Cytokine receptors
- Cytokines
- Inflammation
- Viral
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Neurology
- Clinical Neurology