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The neutrophil interactions with the neurovascular unit entail endothelial dysfunction involving endothelial leakage, formation of edema, coagulation abnormalities, disturbed hemodynamics, tissue infiltration etc. These elements of the \u201cwhole body inflammation,\u201d designated systemic inflammatory response syndrome (SIRS) in conjunction with intracerebral proinflammatory activities, are important triggers of post\u2010traumatic cerebral damage and mortality according to the \u201csecond hit\u201d concept. From the immunologic point of view, the brain is an immune privileged site, known to resist autodestructive inflammatory activity much more efficiently than other organs because of the highly efficient diverse functions of the blood\u2013brain barrier (BBB). However, both the underlying strategy of the BBB to maintain cerebral protecting functions against the post\u2010traumatic neutrophil\u2010mediated \u201csecond hit\u201d and how activated neutrophils may overcome the BBB are currently unknown. Therefore, this review summarizes the current understanding of the \u201csecond hit,\u201d the BBB physiology, and its role in the maintenance of cerebral immune privilege, and discusses recent findings that may explain the pathophysiologic neutrophil\u2013BBB interactions occurring after severe trauma, thus offering novel therapeutic options to protect from post\u2010traumatic brain damage. \u00a9 2006 Wiley Periodicals, Inc. Med Res Rev, 27, No. 3, 401\u2013416, 2007<\/jats:p>","DOI":"10.1002\/med.20064","type":"journal-article","created":{"date-parts":[[2006,6,6]],"date-time":"2006-06-06T21:01:27Z","timestamp":1149627687000},"page":"401-416","source":"Crossref","is-referenced-by-count":113,"title":["Neutrophils and the blood\u2013brain barrier dysfunction after 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