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      Elevated Neutrophil and Presence of Intracranial Artery Stenosis Increase the Risk of Recurrent Stroke

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          Very-late-antigen-4 (VLA-4)-mediated brain invasion by neutrophils leads to interactions with microglia, increased ischemic injury and impaired behavior in experimental stroke.

          Neuronal injury from ischemic stroke is aggravated by invading peripheral immune cells. Early infiltrates of neutrophil granulocytes and T-cells influence the outcome of stroke. So far, however, neither the timing nor the cellular dynamics of neutrophil entry, its consequences for the invaded brain area, or the relative importance of T-cells has been extensively studied in an intravital setting. Here, we have used intravital two-photon microscopy to document neutrophils and brain-resident microglia in mice after induction of experimental stroke. We demonstrated that neutrophils immediately rolled, firmly adhered, and transmigrated at sites of endothelial activation in stroke-affected brain areas. The ensuing neutrophil invasion was associated with local blood-brain barrier breakdown and infarct formation. Brain-resident microglia recognized both endothelial damage and neutrophil invasion. In a cooperative manner, they formed cytoplasmic processes to physically shield activated endothelia and trap infiltrating neutrophils. Interestingly, the systemic blockade of very-late-antigen-4 immediately and very effectively inhibited the endothelial interaction and brain entry of neutrophils. This treatment thereby strongly reduced the ischemic tissue injury and effectively protected the mice from stroke-associated behavioral impairment. Behavioral preservation was also equally well achieved with the antibody-mediated depletion of myeloid cells or specifically neutrophils. In contrast, T-cell depletion more effectively reduced the infarct volume without improving the behavioral performance. Thus, neutrophil invasion of the ischemic brain is rapid, massive, and a key mediator of functional impairment, while peripheral T-cells promote brain damage. Acutely depleting T-cells and inhibiting brain infiltration of neutrophils might, therefore, be a powerful early stroke treatment.
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            Higher neutrophil counts before thrombolysis for cerebral ischemia predict worse outcomes.

            To determine whether higher neutrophil counts before IV recombinant tissue plasminogen activator (rtPA) administration in ischemic stroke (IS) patients are associated with symptomatic intracerebral hemorrhages (sICH) and worse outcomes at 3 months.
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              High neutrophil numbers in human carotid atherosclerotic plaques are associated with characteristics of rupture-prone lesions.

              To score the number of plaque neutrophils and relate the score to plaque morphology and inflammatory status. Neutrophils are inflammatory cells with tissue destruction capabilities that have been found at the site of an atherosclerotic plaque rupture or erosion. Poor evidence exists for neutrophil infiltration in human carotid atherosclerotic plaques, and its association with plaque morphology has not yet been described. A set of 355 human carotid plaques was stained for the neutrophil marker CD66b. High neutrophil numbers were found in plaques with a large lipid core, high macrophage numbers, and low collagen amount and smooth muscle cell numbers. High neutrophil numbers were associated with high interleukin 8 (P<0.001) and matrix metalloproteases 8 (P=0.005) and 9 (P<0.001) plaque levels. High microvessel density within plaques was correlated with high neutrophil numbers (P=0.01). In addition, low numbers of neutrophils were associated with female sex and use of beta-blockers. For the first time to our knowledge, these results show that neutrophil numbers are strongly associated with the histopathologic features of rupture-prone atherosclerotic lesions and suggest a role for neutrophils in plaque destabilization.
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                Author and article information

                Journal
                Stroke
                Stroke
                Ovid Technologies (Wolters Kluwer Health)
                0039-2499
                1524-4628
                October 2018
                October 2018
                : 49
                : 10
                : 2294-2300
                Affiliations
                [1 ]From the Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, China (B.Z., Y.P., J.J., H. Li, X.Z., L.L., Yilong Wang, Yongjun Wang)
                [2 ]Department of Neurology, Taizhou First People’s Hospital, Zhejiang, China (B.Z., Z.W.)
                [3 ]China National Clinical Research Center for Neurological Diseases, Beijing (B.Z., Y.P., J.J., H. Li, X.Z., L.L., Yilong Wang, Yongjun Wang)
                [4 ]Center of Stroke, Beijing Institute for Brain Disorders, China (B.Z., Y.P., J.J., H. Li, X.Z., L.L., Yilong Wang, Yongjun Wang)
                [5 ]Beijing Key Laboratory of Translational Medicine for Cerebrovascular Disease, China (B.Z., Y.P., J.J., H. Li, X.Z., L.L., Yilong Wang, Yongjun Wang)
                [6 ]Department of Neurology and Suzhou Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Jiangsu, China (H. Liu)
                [7 ]Illinois Neurological Institute Stroke Network, Sisters of the Third Order of St. Francis Healthcare System, University of Illinois College of Medicine, Peoria (D.W.)
                [8 ]Dell Medical School, University of Texas at Austin (S.C.J.).
                Article
                10.1161/STROKEAHA.118.022126
                30355101
                aade932b-3936-49f9-b30b-a1629f70a523
                © 2018
                History

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