Mannan-binding lectin deficiency in pediatric patients with inflammatory bowel disease

Abstract

Objective. The incidence of inflammatory bowel disease (IBD) in Europe has increased significantly. At least a fourth of patients are children. Mannan-binding lectin (MBL) is believed to be an important component of innate immunity, acting as an opsonin and activator of the lectin pathway (LP) of complement. The data relating any of the LP factors to IBD are sparse and contradictory and were obtained mainly from adult patients. The aim of this study was to investigate the possible role of MBL in Crohn's disease (CD) and ulcerative colitis (UC) in children. Methods. MBL2 gene single nucleotide polymorphisms (PCR-RFLP) and MBL concentrations (ELISA) were determined. Results. The frequency of MBL2 gene variants responsible for MBL deficiency (LXPA/O and O/O) is significantly higher in CD patients compared with controls or children with UC. A relatively high frequency of the codon 52 mutation (D allele) was noted in these patients. Practically no difference was found between UC and control (C) groups. Similarly, the average MBL levels as well as the number of MBL-deficient (MBL concentrations < 150 ng/ml) individuals differed between CD patients and controls or children suffering from UC. Again, there was no difference between UC and C groups. Conclusions. These data suggest that MBL deficiency may be associated with CD but not with UC in pediatric patients. The possible role of MBL in IBD requires confirmation in larger series and further investigation of the mechanisms involved.

Key Words::

• Crohn's disease
• inflammatory bowel disease
• innate immunity
• mannan-binding lectin
• MBL2
• ulcerative colitis

Acknowledgements

The authors are very grateful to Dr David C. Kilpatrick for his critical reading of the manuscript. This work was partially supported by Medical University of Lodz, Poland, project 502-15-638.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.