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Intracerebroventricular and Intravascular Injection of Viral Particles and Fluorescent Microbeads into the Neonatal Brain
Published on: July 24, 2016
Differential expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in chronic murine
L M Dallasta1, G Wang, R J Bodnar
1Department of Pathology, Division of Neuropathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Insights
In this study of chronic encephalitis, intercellular adhesion molecule-1 (ICAM-1) was found on microglia, but not endothelial cells or astrocytes. This cell-specific expression suggests ICAM-1 may contribute to neurodegeneration in this viral brain infection.
Area of Science:
- Neuroimmunology
- Virology
- Cell Biology
Background:
- Cell adhesion molecules like ICAM-1 and VCAM-1 mediate immune responses in the central nervous system (CNS).
- Pro-inflammatory brain insults, including viral infections, can increase these molecules on brain cells.
Purpose of the Study:
- To investigate the expression of ICAM-1 and VCAM-1 in chronic encephalitis induced by a temperature-sensitive Moloney murine leukemia virus (MoMuLV).
Main Methods:
- Examined viral antigen and adhesion molecule expression in brain tissue during late-stage disease.
- Utilized immunohistochemistry to detect ICAM-1 and VCAM-1 on endothelial cells, astrocytes, and microglia.
Main Results:
- Viral antigen was present in endothelial cells and microglia, but not astrocytes, in affected brain regions.
- ICAM-1 staining was observed on activated microglia, but not endothelial cells or astrocytes.
- No increased VCAM-1 expression was detected in the CNS.
Conclusions:
- Demonstrated cell-specific, differential expression of ICAM-1 and VCAM-1 in MoMuLV (ts-1) encephalitis.
- Lack of endothelial ICAM-1 expression correlates with minimal lymphocytic infiltration.
- Increased microglial ICAM-1 may play a role in MoMuLV (ts-1)-induced neurodegeneration.
Abstract:
The cell adhesion molecules, intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1, are important mediators of immune interactions within the central nervous system (CNS). A wide variety of pro-inflammatory insults to the brain, including viral infection, result in upregulation of these molecules on brain endothelial cells, astrocytes, and microglia. This study investigated the expression of ICAM-1 and VCAM-1 in chronic encephalitis induced by infection with a temperature sensitive (ts-1) strain of Moloney murine leukaemia virus (MoMuLV), an ecotropic murine retrovirus. During the late stages of disease, viral antigen was present in both endothelial cells and microglia, but not astrocytes, in regions of spongiform change and gliosis. In these areas, ICAM-1 staining was detected on activated microglia, but not on endothelial cells or astrocytes. In contrast, no cells showed increased VCAM-1 expression in the CNS. These findings demonstrate that there is cell-specific, differential expression of these adhesion molecules in ts-1 retroviral encephalitis. The lack of endothelial cell expression correlates with the characteristic lack of lymphocytic infiltrate in this chronic retroviral encephalitis and suggests that increased microglial ICAM-1 expression may play a role in the pathogenesis of MoMuLV (ts-1)-mediated neurodegeneration.
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