title: α4 integrin is a regulator of leukocyte recruitment after experimental intracerebral hemorrhage.
abstract: OBJECTIVE
  Intracerebral hemorrhage (ICH) is swiftly followed by an inflammatory response. A key component of this response is the recruitment of leukocytes into the brain, which promotes neurological injury in rodent models. However, the mechanisms by which leukocytes transmigrate across the endothelium into the injured brain are unclear. The present study examines leukocyte adhesion molecules (α4 integrin, L-selectin, and αLβ2 integrin) on 4 leukocyte subtypes to determine which are important for leukocyte recruitment after ICH.
  
  
  METHODS
  We used the blood injection mouse model of ICH, whereby 25 μL of blood was injected into the striatum. Flow cytometry was used to quantify leukocyte populations and adhesion molecule expression in brain and blood. An α4 integrin-blocking antibody was administered to evaluate the contribution of α4 integrin in leukocyte migration and neurological injury.
  
  
  RESULTS
  α4 integrin was elevated on all leukocyte populations in brain after ICH, whereas L-selectin was unchanged and αLβ2 was increased only on T cells. Antagonism of α4 resulted in decreased leukocyte transmigration and lessened neurobehavioral disability.
  
  
  CONCLUSIONS
  α4 integrin is an important cell adhesion molecule involved in neuroinflammation after ICH.
authors.affiliation: From the Department of Neuroscience (M.D.H., Y.A., L.H.S.) and School of Medicine (W.G.A.), University of Connecticut Health Center, Farmington; and Departments of Neurology (L.H.S.) and Neurosurgery (L.H.S.), Hartford Hospital, CT.
authors.forename: Matthew D
authors.initials: MD
authors.lastname: Hammond
authors.affiliation: From the Department of Neuroscience (M.D.H., Y.A., L.H.S.) and School of Medicine (W.G.A.), University of Connecticut Health Center, Farmington; and Departments of Neurology (L.H.S.) and Neurosurgery (L.H.S.), Hartford Hospital, CT.
authors.forename: William G
authors.initials: WG
authors.lastname: Ambler
authors.affiliation: From the Department of Neuroscience (M.D.H., Y.A., L.H.S.) and School of Medicine (W.G.A.), University of Connecticut Health Center, Farmington; and Departments of Neurology (L.H.S.) and Neurosurgery (L.H.S.), Hartford Hospital, CT.
authors.forename: Youxi
authors.initials: Y
authors.lastname: Ai
authors.affiliation: From the Department of Neuroscience (M.D.H., Y.A., L.H.S.) and School of Medicine (W.G.A.), University of Connecticut Health Center, Farmington; and Departments of Neurology (L.H.S.) and Neurosurgery (L.H.S.), Hartford Hospital, CT. Sansing@uchc.edu.
authors.forename: Lauren H
authors.initials: LH
authors.lastname: Sansing
mesh_terms: D000818:Animals; D002543:Cerebral Hemorrhage / Q000276:immunology / Q000378:metabolism*; D007249:Inflammation / Q000276:immunology / Q000378:metabolism; D039441:Integrin alpha4 / Q000378:metabolism*; D019041:L-Selectin / Q000378:metabolism; D007962:Leukocytes / Q000276:immunology / Q000378:metabolism*; D016169:Lymphocyte Function-Associated Antigen-1 / Q000378:metabolism; D051379:Mice; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism
chemical_list: D016169:Lymphocyte Function-Associated Antigen-1; D019041:L-Selectin; D039441:Integrin alpha4
keywords: cell adhesion molecules; cerebral hemorrhage; inflammation; integrins; monocytes