Mannose-Binding Lectins in Cerebrum Development

Zanetta, Jean‐Pierre

doi:10.1007/978-3-642-55557-2_4

Cited by 5 publications

(6 citation statements)

References 72 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Other MBL-mediated mechanisms, closely related to the condition of severe prematurity, in particular to the marked brain immaturity of neonates, may have a role in the genesis of the neurological damage. Studies on the rat cerebellum performed by Zanetta and other authors (26)(27)(28) suggested a role for MBL in the contact guidance of neuronal migration, interneuronal recognition, formation of bridges between migrating neurons and radial astrocytes fibers, myelination and tightening of the ependymal cell barrier, during the ontogenic development of the brain. Based on these evidences, it is conceivable to hypothesize that polymorphisms in the MBL2 gene could suppress these functions, increasing the susceptibility of the brain tissue to various pathogenic insults, as infections and hemorrhages.…”

Section: Articlesmentioning

confidence: 94%

MBL2 gene polymorphisms increase the risk of adverse neurological outcome in preterm infants: a preliminary prospective study

et al. 2014

View full text Add to dashboard Cite

Background: As described in animal models, the lectincomplement pathway is central to the propagation of ischemia-reperfusion injuries in many tissues, including the brain. Similarly, it might affect the genesis of brain damage in preterm infants. MBL2 gene single-nucleotide polymorphisms (SNPs), regulating mannose-binding lectin (MBL) serum levels, could predict the risk of adverse neurological outcome in these infants. Methods: To evaluate the association between SNPs of the MBL2 gene and long-term neurological outcomes in preterm infants, 75 infants (gestational age (GA) ≤ 32 wk) were observed in a prospective longitudinal study and assessed by clinical and instrumental exams at 12 and 24 mo of corrected age (CA). They were genotyped for the promoter polymorphism -221 and for the exon-1 variant alleles (at codons 52, 54, and 57) of the MBL2 gene. results: The MBL2 exon-1 OO genotype was more frequent in children with an adverse neurological outcome (5/35; 7%) than in controls (0/40; 0%), P = 0.045. The risk of intraventricular hemorrhage in carriers of the genotype OO was marked, without reaching statistical significance (odds ratio: 8.67; 95% confidence interval: 0.87-86.06; P = 0.07). conclusion: Preterm infants who are carriers of MBL2 exon-1 OO genotype are exposed to an increased risk of adverse neurological outcomes.

show abstract

Section: Articlesmentioning

confidence: 94%

MBL2 gene polymorphisms increase the risk of adverse neurological outcome in preterm infants: a preliminary prospective study

et al. 2014

View full text Add to dashboard Cite

show abstract

“…If MBL has a protective or harmful role in the physiopathology of the ischemia-reperfusion brain damage is still unclear. According to the studies by Zanetta, we can speculate that MBL may play a protective role in brain development [ 5 ]. Mannose rich glycoproteins markedly accumulate during the second and the third postnatal weeks compared with other monosaccharides and are thereafter degraded.…”

Section: Mbl: Clinical Significancementioning

confidence: 99%

“…Consecutively, MBL could play a critical role in the first line defence during the neonatal period, when the maternal-derived antibodies disappear and the child's own immune system is immature [ 3 , 4 ]. In the same period of life, MBL seems also to play a role in contact guidance of neuronal migration, interneuronal recognition, myelinization, and tightening of the ependymal cell barrier [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

Mannose-Binding Lectin: Biologic Characteristics and Role in the Susceptibility to Infections and Ischemia-Reperfusion Related Injury in Critically Ill Neonates

Auriti

Prencipe

Moriondo

et al. 2017

Journal of Immunology Research

View full text Add to dashboard Cite

The mannose-binding lectin (MBL) is a member of the collectin family, belonging to the innate immunity system. Genetic, biologic, and clinical properties of MBL have been widely investigated throughout the last decades, although some interesting aspects of its potential clinical relevance are still poorly understood. Low circulating concentrations of MBL have been associated with increased risk of infection and poor neurologic outcome in neonates. On the other hand, an excessive and uncontrolled inflammatory response by the neonatal intestine after the exposure to luminal bacteria, leading to an increased production of MBL, may be involved in the onset of necrotizing enterocolitis. The purpose of the present review is to summarize the current knowledge about genetic and biologic characteristics of MBL and its role in the susceptibility to infections and to ischemia-reperfusion related tissue injuries to better explore its clinical relevance during the perinatal period and the possible future therapeutic applications.

show abstract

“…Although MBL has not been studied in a brain injury model, MBL mRNA expression has been detected in brain (Wagner et al, 2003), and MBL and other lectins have been hypothesized to play a role in brain development (Zanetta, 2003).…”

Section: Introductionmentioning

confidence: 99%

Mannose Binding Lectin Gene Deficiency Increases Susceptibility to Traumatic Brain Injury in Mice

Yager

You

Qin

et al. 2008

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

Mannose binding lectin (MBL) initiates complement activation and exacerbates tissue damage after systemic ischemia/reperfusion. We tested the hypothesis that MBL activates complement and worsens outcome using two levels of controlled cortical impact (CCI) in mice. After moderate CCI (0.6 mm depth), MBL immunostaining was detected on injured endothelial cells of wild-type (WT) mice and C3d was detected in MBL KO (deficient in MBL A/C) and WT mice, suggesting that MBL is dispensable for terminal complement activation after CCI. Brain neutrophils, edema, blood-brain barrier permeability, gross histopathology, and motor dysfunction were similar in injured MBL KO and WT mice. In mice subjected to mild CCI (0.2 mm), MBL KO mice had almost two-fold increased acute CA3 cell degeneration at 6 h (P < 0.01 versus WT). Naive MBL KO mice had decreased brain volume but performed similar to WT mice in two distinct Morris water maze (MWM) paradigms. However, injured MBL KO mice had impaired performance in cued platform trials (P < 0.05 versus WT), suggesting a transient nonspatial learning deficit in injured MBL KO mice. The data suggest that MBL deficiency increases susceptibility to CCI through C3-independent mechanisms and that MBL-deficient patients may be at increased risk of poor outcome after traumatic brain injury.

show abstract

Mannose-Binding Lectins in Cerebrum Development

Cited by 5 publications

References 72 publications

MBL2 gene polymorphisms increase the risk of adverse neurological outcome in preterm infants: a preliminary prospective study

MBL2 gene polymorphisms increase the risk of adverse neurological outcome in preterm infants: a preliminary prospective study

Mannose-Binding Lectin: Biologic Characteristics and Role in the Susceptibility to Infections and Ischemia-Reperfusion Related Injury in Critically Ill Neonates

Mannose Binding Lectin Gene Deficiency Increases Susceptibility to Traumatic Brain Injury in Mice

Contact Info

Product

Resources

About