TY - JOUR
T1 - Ficolin-3-mediated lectin complement pathway activation in patients with subarachnoid hemorrhage
AU - Zanier, Elisa R
AU - Zangari, Rosalia
AU - Munthe-Fog, Lea
AU - Hein, Estrid
AU - Zoerle, Tommaso
AU - Conte, Valeria
AU - Orsini, Franca
AU - Tettamanti, Mauro
AU - Stocchetti, Nino
AU - Garred, Peter
AU - De Simoni, Maria-Grazia
PY - 2014/1/14
Y1 - 2014/1/14
N2 - 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.
AB - 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.
KW - Aged
KW - Brain Ischemia
KW - Cohort Studies
KW - Complement Pathway, Mannose-Binding Lectin
KW - Enzyme-Linked Immunosorbent Assay
KW - Female
KW - Glycoproteins
KW - Humans
KW - Lectins
KW - Male
KW - Middle Aged
KW - Neurosurgical Procedures
KW - Prospective Studies
KW - Subarachnoid Hemorrhage
KW - Tomography, X-Ray Computed
KW - Treatment Outcome
KW - Vasospasm, Intracranial
U2 - 10.1212/wnl.0000000000000020
DO - 10.1212/wnl.0000000000000020
M3 - Journal article
C2 - 24336142
SN - 0028-3878
VL - 82
SP - 126
EP - 134
JO - Neurology
JF - Neurology
IS - 2
ER -