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.

Ficolin-3-mediated lectin complement pathway activation in patients with subarachnoid hemorrhage / E.R. Zanier, R. Zangari, L. Munthe-Fog, E. Hein, T. Zoerle, V. Conte, F. Orsini, M. Tettamanti, N. Stocchetti, P. Garred, M. De Simoni. - In: NEUROLOGY. - ISSN 0028-3878. - 82:2(2014 Jan 14), pp. 126-134. [10.1212/WNL.0000000000000020]

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

T. Zoerle;V. Conte;N. Stocchetti;
2014

Abstract

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.
Aged; Brain Ischemia ; Cohort Studies ; Complement Pathway, Mannose-Binding Lectin ; Enzyme-Linked Immunosorbent Assay ; Female; Glycoproteins ; Human s; Lectins ; Male ; Middle Aged ; Neurosurgical Procedures ; Prospective Studies; Subarachnoid Hemorrhage ; Tomography, X-Ray Computed; Treatment Outcome ; Vasospasm, Intracranial; Neurology (clinical) ; Arts and Humanities (miscellaneous)
Settore MED/41 - Anestesiologia
14-gen-2014
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/239776
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