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Titolo:
Intrathecal levels of complement-derived soluble membrane attack complex (sC5b-9) correlate with blood-brain barrier dysfunction in patients with traumatic brain injury
Autore:
Stahel, PF; Morganti-Kossmann, MC; Perez, D; Redaelli, C; Gloor, B; Trentz, O; Kossmann, T;
Indirizzi:
Univ Zurich Hosp, Dept Surg, Div Trauma Surg, CH-8091 Zurich, Switzerland Univ Zurich Hosp Zurich Switzerland CH-8091 CH-8091 Zurich, Switzerland Univ Zurich Hosp, Dept Surg, Div Res, CH-8091 Zurich, Switzerland Univ Zurich Hosp Zurich Switzerland CH-8091 CH-8091 Zurich, Switzerland Univ Hosp Bern, Dept Visceral & Transplantat Surg, Bern, Switzerland Univ Hosp Bern Bern Switzerland & Transplantat Surg, Bern, Switzerland
Titolo Testata:
JOURNAL OF NEUROTRAUMA
fascicolo: 8, volume: 18, anno: 2001,
pagine: 773 - 781
SICI:
0897-7151(200108)18:8<773:ILOCSM>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
CENTRAL-NERVOUS-SYSTEM; ACTIVATED TERMINAL COMPLEMENT; CEREBROSPINAL-FLUID; NEUROLOGICAL DISORDERS; MULTIPLE-SCLEROSIS; IGG ANALYSES; HEAD-INJURY; INTERLEUKIN-8; EXPRESSION; PRINCIPLES;
Keywords:
blood-brain barrier; cerebrospinal fluid; complement; membrane attack complex; traumatic brain injury;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Stahel, PF Univ Zurich Hosp, Dept Surg, Div Trauma Surg, CH-8091 Zurich, Switzerland Univ Zurich Hosp Zurich Switzerland CH-8091 rich, Switzerland
Citazione:
P.F. Stahel et al., "Intrathecal levels of complement-derived soluble membrane attack complex (sC5b-9) correlate with blood-brain barrier dysfunction in patients with traumatic brain injury", J NEUROTRAU, 18(8), 2001, pp. 773-781

Abstract

It has become evident in recent years that intracranial inflammation aftertraumatic brain injury (TBI) is, at least in part, mediated by activation of the complement system. However, most conclusions have been drawn from experimental studies, and the intrathecal activation of the complement cascade after TBI has not yet been demonstrated in humans. In the present study, we analyzed the levels of the soluble terminal complement complex sC5b-9 byELISA in ventricular cerebrospinal fluid (CSF) of patients with severe TBI(n = 11) for up to 10 days after trauma. The mean sC5b-9 levels in CSF were significantly elevated in 10 of 11 TBI patients compared to control CSF from subjects without trauma or inflammatory neurological disease (n = 12; p< 0.001). In some patients, the maximal sC5b-9 concentrations were up to 1,800-fold higher than in control CSF. The analysis of the extent of posttraumatic blood-brain barrier (BBB) dysfunction, as determined by CSF/serum albumin quotient (Q(A)), revealed that patients with a moderate to severe BBBimpairment (mean Q(A) > 0.01) had significantly higher intrathecal sC5b-9 levels as compared to patients with normal BBB function (mean Q(A) < 0.007;p < 0.0001). In addition, a significant correlation between the individualdaily Q(A) values and the corresponding sC5b-9 CSF levels was detected in 8 of 11 patients (r = 0.72-0.998; p < 0.05). These data demonstrate for thefirst time that terminal pathway complement activation occurs after head injury and suggest a possible pathophysiological role of complement with regard to posttraumatic BBB dysfunction.

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Documento generato il 25/01/20 alle ore 16:46:23