Mannose-Binding Lectin Deficiency and Its Impact on Pulmonary Morbidity in Children

Kathrin W Dahl1, Frederik Buchvald1, Astrid Thomas1

  • 1Pediatric Pulmonary Service, Department of Paediatric & Adolescent Medicine, Rigshospitalet, Copenhagen, Denmark.

Insights

Mannose-binding lectin (MBL) deficiency, linked to MBL2 gene variations, did not show an association with increased pulmonary morbidity in children with recurrent lung infections. MBL genotyping is unlikely to be a sole factor in identifying pulmonary issues in these children.

Area of Science:

  • Immunology
  • Pediatrics
  • Genetics

Background:

  • Mannose-binding lectin (MBL) deficiency, caused by MBL2 gene polymorphisms, is suspected to increase susceptibility to respiratory infections in children.
  • Recurrent pulmonary infections in children often lack a clear cause, prompting investigation into genetic factors.

Purpose of the Study:

  • To investigate the association between MBL deficiency and pulmonary morbidity in children experiencing recurrent pulmonary infections of unknown origin.

Main Methods:

  • A retrospective, cross-sectional study included 113 children with recurrent pulmonary infections and known MBL2 genotypes.
  • Pulmonary morbidity was assessed using lung function tests, BMI, antibiotic prescriptions, and radiological lung changes (X-ray/CT).

Main Results:

  • No significant differences in lung function, BMI, or antibiotic use were found between high- and low-expression MBL2 genotypes.
  • The odds of structural lung changes were not related to MBL2 genotypes.
  • Pulmonary morbidity was not associated with low-expression MBL2 genotypes in this selected pediatric group.

Conclusions:

  • MBL deficiency is not a significant factor in pulmonary morbidity among children with recurrent, unexplained pulmonary infections.
  • MBL genotyping alone is insufficient to explain differences in pulmonary morbidity in this patient population.