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Abstract
Neurotropic recombinant strain of Mouse Hepatitis Virus, RSA59, induces meningo-encephalitis, myelitis and demyelination following intracranial inoculation. RSA59 induced neuropathology is partially caused by activation of CNS resident microglia, as demonstrated by changes in cellular morphology and increased expression of a microglia/macrophage specific calcium ion binding factor, Iba1. Affymetrix Microarray analysis for mRNA expression data reveals expression of inflammatory mediators that are known to be released by activated microglia. Microglia-specific cell surface molecules, including CD11b, CD74, CD52 and CD68, are significantly upregulated in contrast to CD4, CD8 and CD19. Protein analysis of spinal cord extracts taken from mice 6 days post-inoculation, the time of peak inflammation, reveals robust expression of IFN-γ, IL-12 and mKC. Data suggest that activated microglia and inflammatory mediators contribute to a local CNS microenvironment that regulates viral replication and IFN-γ production during the acute phase of infection, which in turn can cause phagolysosome maturation and phagocytosis of the myelin sheath, leading to demyelination.
Highlights
There is a fundamental distinction between acute and chronic inflammation in various pathological studies
The current mRNA profiling data demonstrates significant upregulation of genes involved in innate immune responses during acute Mouse hepatitis virus (MHV) infection
As they are consistent with histopathological data demonstrating the activation of microglia and innate immune response in central nervous system (CNS) tissues following intracranial inoculation
Summary
There is a fundamental distinction between acute and chronic inflammation in various pathological studies. Acute inflammation comprises the immediate and early response to an injurious agent and is basically a defensive response that paves the way for repair of the damaged site. Neuroinflammation revolves around direct neuro-glial cell responses (host cell factors) which are induced by infection and injury within the CNS. It involves the mechanism by which these responses contribute to neuropathology and neurobiology of diseases. Previous studies demonstrated that microglia can be persistently infected by neurotropic strains of Mouse hepatitis virus (MHV) [2]
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