Neuroscience 2001 Abstract
| Presentation Number: | 659.18 |
|---|---|
| Abstract Title: | Genetic Manipulation of Monocyte Chemoattractant Protein-1 (MCP-1) and its Receptor (CCR2) alters Cytokine and Chemokine Gene Expression Profiles in Response to Cortical Injury. |
| Authors: |
Muessel, M. J.*1
; Klein, R. M.1
; Wilson, A. M.1
; Berman, N. E. J.1
1Dept Anat & Cell Biol, Univ of Kansas Med Ctr, Kansas City, KS |
| Primary Theme and Topics |
Neurological and Psychiatric Conditions - Neuroimmunology and Infections |
| Secondary Theme and Topics | Neurological and Psychiatric Conditions<br />- Genetic Models |
| Session: |
659. Neuroimmunology and infections: inflammation I Poster |
| Presentation Time: | Tuesday, November 13, 2001 2:00 PM-3:00 PM |
| Location: | Exhibit Hall YY-10 |
| Keywords: | chemokines, brain injury, cytokines, knockout mice |
MCP-1, a β-chemokine (chemoattractant cytokine), can regulate T cell differentiation and the balance between Th1 and Th2 cytokine expression. MCP-1 also directs monocyte infiltration following injury and/or inflammation. MCP-1 -/- and CCR2 -/- mice show altered retrograde neuronal degeneration in the thalamus following visual cortical injury with delayed cell death in MCP-1 -/- (SFN Abstr.26: 328, 2000). In the present study we analyzed thalamic chemokine/cytokine gene expression at 0, 24 and 72 hours after removal of the visual cortex in MCP-1 -/- and CCR2 -/- and wildtype mice. The data indicated that RANTES, interferon (IFN)-gamma(γ), and macrophage inflammatory protein (MIP)-1 alpha (α) were elevated in MCP-1 -/- compared to wildtype mice following injury. MIP-1α mRNA was also elevated in the CCR2 -/- compared to wildtype. At 24 hours following cortical injury, tumor necrosis factor-alpha (TNF-α) mRNA was signficantly elevated in MCP-1 -/-; TNF-α protein was elevated in all 3 strains of mice. TNFR1 mRNA was elevated in all 3 strains, however, MCP-1 -/- have higher levels than wild type or CCR2 -/- mice. The thalamic cytokine/chemokine profile as well as the cytokine response to injury is altered by ablation of MCP-1 or its primary receptor (CCR2). The elevated levels of IFN-γ and TNF strongly suggest that in the absence of MCP-1, the Th1/Th2 balance in the thalamus is shifted. The alteration of cytokine expression may relate directly to the delayed cell death observed in MCP-1 -/-.
Supported by NS38282 and HD02528
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2001 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2001. Online.
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