title: [Inflammatory response during ischaemic processes: adhesion molecules and immunomodulation].
abstract: BACKGROUND
  After cerebral ischemia, necrotic cell death occurs specially for neurons, mainly due to the deprivation of oxygen and glucose. Cell necrosis triggers the activation of the immune system followed by an inflammatory response. This reaction is characterized by the activation of astrocytes and microglia together with the infiltration of peripheral immune cells.
  
  
  METHODS
  Both, microglia and inflammatory cells, including circulating peripheral inflammatory cells, get activated and release a plethora of inflammatory mediators, cytokines, chemokines, etc. Such released factors induce the overexpression of adhesion molecules, increasing the blood brain barrier permeability, thus favoring even more inflammatory cell infiltration. In the end, this contributes to increase brain damage. Inflammatory response is nevertheless necessary in order to eliminate cellular debris from both apoptotic and necrotic cells. It seems to be also implicated in the initiation of certain mechanisms responsible for brain repair and plasticity. As a result, the inflammatory response is a coordinated effort. Activation of inflammation triggers an immunosuppressant and anti-inflammatory response. A high rate of infections in patients suffering from stroke, together with increased serum levels of anti-inflammatory molecules in these patients, support this statement. The anti-inflammatory response could be interpreted as the organism attempting to control the heightened inflammatory response that occurs after cerebral ischemia. On the other hand, following an ischemic event, there are several new cerebral epitopes that get exposed to the immune system, which would never have been exposed under normal physiological conditions.
  
  
  CONCLUSIONS
  Therefore immunosuppression after an ischemic accident hinders the development of auto-immune responses.
authors.affiliation: Laboratorio de Investigación de Neurociencias Clínicas, Servicio de Neurología, Hospital Clínico Universitario, Universidad de Santiago de Compostela, España.
authors.forename: María D
authors.initials: MD
authors.lastname: Cuenca-López
authors.forename: David
authors.initials: D
authors.lastname: Brea
authors.forename: María F
authors.initials: MF
authors.lastname: Galindo
authors.forename: David
authors.initials: D
authors.lastname: Antón-Martínez
authors.forename: María J
authors.initials: MJ
authors.lastname: Sanz
authors.forename: Jesús
authors.initials: J
authors.lastname: Agulla
authors.forename: José
authors.initials: J
authors.lastname: Castillo
authors.forename: Joaquín
authors.initials: J
authors.lastname: Jordán
mesh_terms: D056704:Adaptive Immunity / Q000276:immunology; D015551:Autoimmunity / Q000276:immunology*; D002545:Brain Ischemia / Q000276:immunology*; D015815:Cell Adhesion Molecules / Q000276:immunology*; D016923:Cell Death; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology; D007136:Immunoglobulins / Q000276:immunology; D056747:Immunomodulation; D007249:Inflammation / Q000276:immunology*; D016023:Integrins / Q000276:immunology; D017628:Microglia / Q000276:immunology; D009474:Neurons / Q000276:immunology; D019087:Selectins / Q000276:immunology
chemical_list: D015815:Cell Adhesion Molecules; D007136:Immunoglobulins; D016023:Integrins; D019087:Selectins