Overexpression of Monocyte Chemoattractant Protein 1 in the Brain Exacerbates Ischemic Brain Injury and is Associated with Recruitment of Inflammatory Cells

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  • Yong Chen
    Stroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland
  • John M. Hallenbeck
    Stroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland
  • Christl Ruetzler
    Stroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland
  • David Bol
    Bristol-Myers Squibb, Princeton, New Jersey
  • Karen Thomas
    Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, Maryland
  • Nancy E. J. Berman
    Department of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City, Kansas, U.S.A.
  • Stefanie N. Vogel
    Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, Maryland

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<jats:p> Brain cells produce cytokines and chemokines during the inflammatory process after stroke both in animal models and in patients. Monocyte chemoattractant protein 1 (MCP-1), one of the proinflammatory chemokines, can attract monocytes to the tissue where MCP-1 is overexpressed. However, the role of MCP-1 elevation in stroke has not been explored in detail. The authors hypothesized that elevated MCP-1 levels would lead to increased influx of monocytes and increased brain infarction size in stroke induced by middle cerebral artery occlusion with partial reperfusion. There were no differences in blood pressure, blood flow, or vascular architecture between wild-type mice and transgenic MBP-JE mice. Twenty-four to 48 hours after middle cerebral artery occlusion, brain infarction volumes after ischemia were significantly larger in MBP-JE mice than in wild-type controls and were accompanied by increased local transmigration and perivascular accumulation of macrophages and neutrophils. These results indicate that MCP-1 can contribute to inflammatory injury in stroke. </jats:p>

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