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aprotectiveroleforelrchemokinesduringacuteviralencephalomyelitis的保护作用elr趋化因子在急性病毒性脑脊髓炎
A Protective Role for ELR+ Chemokines during Acute
Viral Encephalomyelitis
1 2 2 1,3
Martin P. Hosking , Liping Liu , Richard M. Ransohoff , Thomas E. Lane *
1 Department of Molecular Biology and Biochemistry, University of California, Irvine, California, United States of America, 2 Neuroinflammation Research Center,
Department of Neurosciences, Cleveland Clinic, Cleveland, Ohio, United States of America, 3 Institute for Immunology, Infectious Diseases, and Vaccines, University of
California, Irvine, California, United States of America
Abstract
The functional role of ELR-positive CXC chemokines in host defense during acute viral-induced encephalomyelitis was
determined. Inoculation of the neurotropic JHM strain of mouse hepatitis virus (JHMV) into the central nervous system (CNS)
of mice resulted in the rapid mobilization of PMNs expressing the chemokine receptor CXCR2 into the blood. Migration of
PMNs to the CNS coincided with increased expression of transcripts specific for the CXCR2 ELR-positive chemokine ligands
CXCL1, CXCL2, and CXCL5 within the brain. Treatment of JHMV-infected mice with anti-CXCR2 blocking antibody reduced
PMN trafficking into the CNS by .95%, dampened MMP-9 activity, and abrogated blood-brain-barrier (BBB) breakdown.
Correspondingly, CXCR2 neutralization resulted in diminished infiltration of virus-specific T cells, an inability to control viral
replication within the brain, and 100% mortality. Blocking CXCR2 signaling did not impair the generation of virus-specific T
cells, indicating that CXCR2 is not required to tailor anti-JHMV T cell responses. Evaluation of mice in which CXCR2 is
genetically silenced (CXCR22/ 2 mice) confirmed that PMNs neither expressed CXCR2 nor migrated
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