Neuroscience 2005 Abstract
Presentation Number: | 585.9 |
---|---|
Abstract Title: | Direct evidence that activating the interleukin 1 type I receptor enhances ischemic brain damage. |
Authors: |
Lazovic, J.*1
; Basu, A.2
; Rothstein, R. P.
; Smith, M. B.
; Levison, S. W.
1Clinic for Special Children, Strasburg, PA 2India, 535 Bunker Hill Rd, 17579, |
Primary Theme and Topics |
Disorders of the Nervous System - Neurotoxicity, Inflammation, and Neuroprotection -- Neuroinflammation |
Session: |
585. Neuroinflammation Slide |
Presentation Time: | Tuesday, November 15, 2005 10:00 AM-10:15 AM |
Location: | Washington Convention Center - Room 149A |
Keywords: | neuroinflammation, IL-1 receptor, MRI |
Recovery from ischemic brain damage is affected by many variables that include neuroinflammation. Proinflammatory cytokines such as IL-1 can exacerbate the extent of damage subsequent to ischemia, however, the receptor(s) that mediates its effects remains unclear. To establish whether the IL-1 type 1 receptor (IL-1R1) is necessary for IL-1 to exacerbate brain damage we employed a modified Levine model of H/I on adult mice and used T2-weighted magnetic resonance imaging (MRI) at 24 h to assess the initial extent of the hyperintense T2 signal. At 48 h wild type (WT) and IL-1R1 null animals were injected with 2 ng recombinant murine IL-1β into the ventricle of the undamaged hemisphere. MR imaging was repeated at 7 days (after H/I) to evaluate the final volume of ischemic brain damage. At 7 days following H/I, the volume of the hyperintense T2-signal at 7 days in WT animals injected with IL-1β was increased 8% compared to the initial damage volume at 24 h. By contrast, the volume of the hyperintense T2-signal in IL-1R1 null animals injected with IL-1β was reduced compared to the initial damage volume at 24 h. The difference in preserved brain tissue between IL-1R1 null and WT animals injected with IL-1β was statistically significant (p <0.05). At the cellular level at 72 h, fewer amoeboid microglia/macrophages and fewer GFAP-positive cells were present in the neocortex of IL-1R1 null mice compared to WT mice following the IL-1β injections. There was no noticeable difference in the numbers of reactive microglia and astrocytes in the striatum. Our findings indicate that therapeutic modalities aimed toward suppression of IL-1R1 signaling may hold promise to preserve neocortical function after stroke.
Supported by MH 59950 (SWL) and HD 30705 (SWL and MBS)
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2005 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2005. Online.
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