TY - JOUR
T1 - Mannose Binding Lectin, S100 B Protein, and Brain Injuries in Neonates With Perinatal Asphyxia
AU - Auriti, Cinzia
AU - Prencipe, Giusi
AU - Inglese, Rita
AU - Moriondo, Maria
AU - Nieddu, Francesco
AU - Mondı̀, Vito
AU - Longo, Daniela
AU - Bucci, Silvia
AU - Del Pinto, Tamara
AU - Timelli, Laura
AU - Di Ciommo, Vincenzo Maria
N1 - Funding Information:
Thanks to Dr. Rachel Bell, Ph.D., Bioscript Medical, Macclesfield, UK, for her valuable collaboration in reviewing the manuscript for the English language. Funding. The promoter of the research was Bambino Ges? Children's Hospital, in Rome, through a research grant, code N? 201703p004152, concerning laboratory determinations and statistical analysis of data. Genetics was performed at Meyer Institute in Florence based on an unpaid collaboration agreement.
Publisher Copyright:
© Copyright © 2020 Auriti, Prencipe, Inglese, Moriondo, Nieddu, Mondı̀, Longo, Bucci, Del Pinto, Timelli and Di Ciommo.
PY - 2020/9/17
Y1 - 2020/9/17
N2 - Perinatal asphyxia triggers an acute inflammatory response in the injured brain. Complement activation and neuroinflammation worsen brain damage after a systemic ischemia/reperfusion insult. The increase of mannose binding lectin (MBL) during asphyxia may contribute to the brain damage, via activation of the complement lectin pathway. The possible role of MBL2 gene variants in influencing the severity of post-asphyxia brain injuries is still unexplored. This retrospective study included 53 asphyxiated neonates: 42 underwent therapeutic hypothermia (TH) and 11 did not because they were admitted to the NICU later than 6 h after the hypoxic insult. Blood samples from TH-treated and untreated patients were genotyped for MBL2 gene variants, and biomarker plasma levels (MBL and S100 B protein) were measured at different time points: during hypothermia, during rewarming, and at 7–10 days of life. The timing of blood sampling, except for the T1 sample, was the same in untreated infants. Highest (peak) levels of MBL and MBL2 genotypes were correlated to neuroimaging brain damage or death and long-term neurodevelopmental delay. MBL2 wild-type genotype was associated with the highest MBL levels and worst brain damage on MRI (p = 0.046) at 7–10 days after hypoxia. MBL increased in both groups and S100B decreased, slightly more in treated than in untreated neonates. The progressive increase of MBL (p = 0.08) and to be untreated with TH (p = 0.08) increased the risk of brain damage or death at 7–10 days of life, without affecting neurodevelopmental outcomes at 1 year. The effect of TH on MBL plasma profiles is uncertain.
AB - Perinatal asphyxia triggers an acute inflammatory response in the injured brain. Complement activation and neuroinflammation worsen brain damage after a systemic ischemia/reperfusion insult. The increase of mannose binding lectin (MBL) during asphyxia may contribute to the brain damage, via activation of the complement lectin pathway. The possible role of MBL2 gene variants in influencing the severity of post-asphyxia brain injuries is still unexplored. This retrospective study included 53 asphyxiated neonates: 42 underwent therapeutic hypothermia (TH) and 11 did not because they were admitted to the NICU later than 6 h after the hypoxic insult. Blood samples from TH-treated and untreated patients were genotyped for MBL2 gene variants, and biomarker plasma levels (MBL and S100 B protein) were measured at different time points: during hypothermia, during rewarming, and at 7–10 days of life. The timing of blood sampling, except for the T1 sample, was the same in untreated infants. Highest (peak) levels of MBL and MBL2 genotypes were correlated to neuroimaging brain damage or death and long-term neurodevelopmental delay. MBL2 wild-type genotype was associated with the highest MBL levels and worst brain damage on MRI (p = 0.046) at 7–10 days after hypoxia. MBL increased in both groups and S100B decreased, slightly more in treated than in untreated neonates. The progressive increase of MBL (p = 0.08) and to be untreated with TH (p = 0.08) increased the risk of brain damage or death at 7–10 days of life, without affecting neurodevelopmental outcomes at 1 year. The effect of TH on MBL plasma profiles is uncertain.
KW - genotype
KW - mannose binding lectin
KW - perinatal asphyxia
KW - S100B protein
KW - therapeutic hypothermia
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U2 - 10.3389/fped.2020.00527
DO - 10.3389/fped.2020.00527
M3 - Article
AN - SCOPUS:85091891848
VL - 8
JO - Frontiers in Pediatrics
JF - Frontiers in Pediatrics
SN - 2296-2360
M1 - 527
ER -