TY - JOUR
T1 - The complement lectin pathway after cardiac arrest
AU - Haugaard, Simon Foged
AU - Jeppesen, Anni Nørgaard
AU - Troldborg, Anne
AU - Kirkegaard, Hans
AU - Thiel, Steffen
AU - Hvas, Anne-Mette
N1 - This article is protected by copyright. All rights reserved.
PY - 2018/8
Y1 - 2018/8
N2 - The lectin pathway (LP) of the complement system may initiate inflammatory reactions when body tissue is altered. We aimed to investigate the levels of the LP proteins in out-of-hospital cardiac arrest patients, and to compare these with healthy individuals. Furthermore, we aimed to clarify whether the duration of targeted temperature management influenced LP protein levels, and we further examined whether LP proteins were associated with 30-day mortality. We included 82 patients resuscitated from out-of-hospital cardiac arrest. The patients were randomly assigned to 24 or 48 hours of targeted temperature management at 33 ± 1°C. Blood samples were obtained 22, 46 and 70 hours after target temperature was reached. Levels of the LP proteins (mannan-binding lectin [MBL], M-ficolin, H-ficolin, collectin liver 1 [CL-L1], MBL-associated serine protease 1 [MASP-1], MASP-2, MASP-3 and MBL-associated protein of 44 kDa [MAp44]) were measured using time-resolved immunofluorometric assays. Data from 82 gender matched healthy individuals were used for comparison. Levels of CL-L1, MASP-1, MASP-2 and MAp44 were significantly higher, whereas M-ficolin levels were significantly lower in cardiac arrest patients compared with healthy individuals. MASP-2, MASP-3 and M-ficolin levels changed significantly when comparing 24 and 48 hours of targeted temperature management. The LP protein levels were not different between 30-day survivors and non-survivors after cardiac arrest. The differences in LP protein levels between patients and healthy individuals may indicate that cardiac arrest patients have an activated LP. Overall, the LP protein levels were not influenced by the duration of targeted temperature management, and the levels were not associated with 30-day mortality.
AB - The lectin pathway (LP) of the complement system may initiate inflammatory reactions when body tissue is altered. We aimed to investigate the levels of the LP proteins in out-of-hospital cardiac arrest patients, and to compare these with healthy individuals. Furthermore, we aimed to clarify whether the duration of targeted temperature management influenced LP protein levels, and we further examined whether LP proteins were associated with 30-day mortality. We included 82 patients resuscitated from out-of-hospital cardiac arrest. The patients were randomly assigned to 24 or 48 hours of targeted temperature management at 33 ± 1°C. Blood samples were obtained 22, 46 and 70 hours after target temperature was reached. Levels of the LP proteins (mannan-binding lectin [MBL], M-ficolin, H-ficolin, collectin liver 1 [CL-L1], MBL-associated serine protease 1 [MASP-1], MASP-2, MASP-3 and MBL-associated protein of 44 kDa [MAp44]) were measured using time-resolved immunofluorometric assays. Data from 82 gender matched healthy individuals were used for comparison. Levels of CL-L1, MASP-1, MASP-2 and MAp44 were significantly higher, whereas M-ficolin levels were significantly lower in cardiac arrest patients compared with healthy individuals. MASP-2, MASP-3 and M-ficolin levels changed significantly when comparing 24 and 48 hours of targeted temperature management. The LP protein levels were not different between 30-day survivors and non-survivors after cardiac arrest. The differences in LP protein levels between patients and healthy individuals may indicate that cardiac arrest patients have an activated LP. Overall, the LP protein levels were not influenced by the duration of targeted temperature management, and the levels were not associated with 30-day mortality.
KW - complement
KW - human
KW - inflammation
KW - molecules
KW - processes
KW - subject
UR - http://www.scopus.com/inward/record.url?scp=85050309111&partnerID=8YFLogxK
U2 - 10.1111/sji.12680
DO - 10.1111/sji.12680
M3 - Journal article
C2 - 29885250
SN - 0300-9475
VL - 88
SP - e12680
JO - Scandinavian Journal of Immunology
JF - Scandinavian Journal of Immunology
IS - 2
M1 - 12680
ER -