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Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
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The chemokine receptor CXCR2 and coronavirus-induced neurologic disease

Jason G Weinger1, Brett S Marro, Martin P Hosking

  • 1Department of Molecular Biology & Biochemistry, UC Irvine, CA 92697-3900, USA.

Virology
|December 11, 2012
PubMed

Insights

The chemokine receptor CXCR2 plays a crucial role in defending the central nervous system (CNS) against mouse hepatitis virus (MHV) infection by recruiting immune cells and protecting glial cells, despite persistent viral infection and demyelination.

Area of Science:

  • Neuroimmunology
  • Virology
  • Cellular and Molecular Neuroscience

Background:

  • Mouse hepatitis virus (MHV) causes acute encephalomyelitis in mice, primarily infecting glial cells and leading to chronic neuroinflammation and demyelination.
  • While T cells control acute viral replication, they do not achieve sterile immunity, allowing persistent MHV infection.
  • The chemokine receptor CXCR2 is implicated in host defense mechanisms within the CNS.

Purpose of the Study:

  • To investigate the role of CXCR2 in the host response to MHV infection in the CNS.
  • To understand how CXCR2 influences myeloid cell recruitment and glial cell survival during MHV-induced neuroinflammation.

Main Methods:

  • Inoculation of susceptible mice with the neurotropic JHM strain of MHV.
  • Analysis of viral replication, immune cell infiltration, and glial cell survival in the CNS.
  • Assessment of CXCR2 expression and function in response to MHV infection.

Main Results:

  • MHV preferentially replicates in glial cells within the CNS.
  • CXCR2 signaling promotes the recruitment of myeloid cells to the CNS.
  • CXCR2 activation protects oligodendroglia from cytokine-mediated death during MHV infection.

Conclusions:

  • CXCR2 plays a critical role in mediating host defense against MHV-induced neuroinflammation.
  • CXCR2 contributes to the recruitment of protective myeloid cells and the survival of oligodendroglia.
  • Targeting CXCR2 may offer therapeutic strategies for neuroinflammatory diseases like those caused by MHV.

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