title: Serum mannose-binding lectin (MBL) gene polymorphism and low MBL levels are associated with neonatal sepsis and pneumonia.
abstract: OBJECTIVE
  The aim of this study was to determine the serum mannose-binding lectin (MBL) levels and the frequency of MBL gene polymorphisms in infants with neonatal sepsis.
  
  
  METHODS
  Between January 2008 and January 2010, a total of 93 infants were included in this study and 53 of them had neonatal sepsis diagnosis as study group and 40 infants who had no sepsis according to clinical and laboratory findings as control group.
  
  
  RESULTS
  Serum MBL levels were found to be low in 17 of 93 infants. Eleven of them were in the sepsis group and six of them were in the control group. Serum MBL levels were significantly lower in infants with sepsis compared with the control group. Frequencies of genotype AB and BB were also significantly higher in the study group compared with the control group. Most importantly, presence of B allele of MBL exon 1 gene was found to be associated with an increased risk for neonatal sepsis. Additionally, in the study group, the mean serum MBL levels were found to be significantly lower in the premature infants compared with the term infants. Pneumonia, bronchopulmonary dysplasia (BPD) and intraventricular hemorrhage (IVH) were significantly higher in infants with MBL deficiency compared with infants with normal MBL levels.
  
  
  CONCLUSIONS
  Low MBL levels and presence of B allele of MBL exon 1 gene were found to be important risk factors for development of both neonatal sepsis and pneumonia, especially in premature infants. Low MBL levels and MBL gene polymorphisms might also be associated with inflammation-related neonatal morbidities such as BPD and IVH.
authors.affiliation: Division of Neonatology, Department of Pediatrics, Uludag University School of Medicine, Bursa, Turkey.
authors.forename: H
authors.initials: H
authors.lastname: Özkan
authors.forename: N
authors.initials: N
authors.lastname: Köksal
authors.forename: M
authors.initials: M
authors.lastname: Çetinkaya
authors.forename: Ş
authors.initials: Ş
authors.lastname: Kiliç
authors.forename: S
authors.initials: S
authors.lastname: Çelebi
authors.forename: B
authors.initials: B
authors.lastname: Oral
authors.forename: F
authors.initials: F
authors.lastname: Budak
mesh_terms: D016022:Case-Control Studies; D005260:Female; D020022:Genetic Predisposition to Disease; D060005:Genotyping Techniques; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007234:Infant, Premature / Q000097:blood; D007235:Infant, Premature, Diseases / Q000097:blood / Q000235:genetics*; D015931:Intensive Care, Neonatal; D008297:Male; D037601:Mannose-Binding Lectin / Q000097:blood / Q000235:genetics*; D011014:Pneumonia / Q000097:blood / Q000235:genetics*; D011110:Polymorphism, Genetic; D012307:Risk Factors; D018805:Sepsis / Q000097:blood / Q000235:genetics*
chemical_list: D037601:Mannose-Binding Lectin