📄 CXCR2 signaling and host defense following coronavirus-induced encephalomyelitis

Inoculation of the neurotropic JHM strain of mouse hepatitis virus (JHMV) into the CNS of susceptible strains of mice results in widespread replication within glial cells, accompanied by infiltration of virus-specific T lymphocytes that control the virus through cytokine secretion and cytolytic activity. The virus persists within the white matter tracts of surviving mice, resulting in demyelination that is amplified by inflammatory T cells and macrophages. In response to infection, numerous cytokines/chemokines are secreted by resident cells of the CNS and inflammatory leukocytes that participate in both host defense and disease. Among these are the ELR-positive chemokines that are able to signal through CXC chemokine receptors including CXCR2. Shortly after JHMV infection, ELR-positive chemokines contribute to host defense by attracting CXCR2-expressing cells, including polymorphonuclear cells, to the CNS that aid host defense by increasing the permeability of the blood-brain barrier. During chronic disease, CXCR2 signaling on oligodendroglia protects these cells from apoptosis and restricts the severity of demyelination. This review covers aspects related to host defense and disease in response to JHMV infection and highlights the different roles of CXCR2 signaling in these processes. © 2012 Future Medicine Ltd.

keywords 🔗 white matter (16) 🔗 hepatitis virus (437) 🔗 mouse hepatitis (371)

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