Ficolin-3-mediated lectin complement pathway activation in patients with subarachnoid hemorrhage.

Autor:	Zanier ER; From the IRCCS-Istituto di Ricerche Farmacologiche Mario Negri (E.R.Z., R.Z., F.O., M.T., M.-G.D.S.), Department of Neuroscience, Milan; Department of Physiopathology and Transplant, Milan University and Neuro ICU (R.Z., T.Z., V.C., N.S.), Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico, Milan, Italy; and Laboratory of Molecular Medicine (L.M.-F., E.H., P.G.), Department of Clinical Immunology, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, Denmark., Zangari R, Munthe-Fog L, Hein E, Zoerle T, Conte V, Orsini F, Tettamanti M, Stocchetti N, Garred P, De Simoni MG
Jazyk:	angličtina
Zdroj:	Neurology [Neurology] 2014 Jan 14; Vol. 82 (2), pp. 126-34. Date of Electronic Publication: 2013 Dec 11.
DOI:	10.1212/WNL.0000000000000020
Abstrakt:	Objectives: To assess the involvement of ficolin-3, the main initiator of the lectin complement pathway (LCP), in subarachnoid hemorrhage (SAH) pathology and outcome. Methods: In this preliminary exploratory study, plasma concentration of ficolin-3 and of ficolin-3-mediated functional LCP activity was measured, along with that of other LCP initiators (mannose-binding lectin, ficolin-2, and ficolin-1), C3 activation products, and soluble C5b-9 terminal complex, in a prospective cohort of 39 patients with SAH and 20 healthy controls. The following parameters were recorded: SAH severity, assessed using the World Federation of Neurosurgical Societies grading scale; vasospasm, defined as neuro-worsening with angiographic confirmation of vessel narrowing; cerebral ischemia, defined as hypodense lesion on CT scan performed before discharge; and 6-month outcome, assessed using the Glasgow Outcome Scale. Results: In patients, no changes were detected for ficolin-3 compared with controls. Notably, however, ficolin-3-mediated functional LCP activity was reduced. Low levels of plasma ficolin-3 and ficolin-3-mediated functional LCP activity were related to SAH severity, vasospasm, and cerebral ischemia. Moreover, ficolin-3 functional LCP activity was decreased in patients with unfavorable outcome. Conclusion: Our data provide evidence that LCP is activated after SAH and that the actual plasma concentrations of ficolin-3 reflect the severity of brain injury as evaluated by clinical and structural parameters. These results support the idea that ficolin-3-mediated functional LCP activity may be targeted to control injury progression in SAH.
Databáze:	MEDLINE
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