Related Experiment Video
Updated: Aug 11, 2026

Antibody Binding Specificity for Kappa (Vκ) Light Chain-containing Human (IgM) Antibodies: Polysialic Acid (PSA) Attached to NCAM as a Case Study
Published on: June 29, 2016
Mannan-binding lectin in children with chronic gastritis
L Bak-Romaniszyn1, M Cedzyński, J Szemraj
1Department of Paediatrics, Preventive Cardiology and Clinical Immunology, Medical University of Łódź, Łódź, Poland.
Insights
Mannan-binding lectin (MBL) insufficiency does not appear to increase the risk of chronic gastritis in children. However, MBL
Area of Science:
- Immunology
- Pediatric Gastroenterology
Background:
- Chronic gastritis (CG) in children is a significant health concern.
- The role of mannan-binding lectin (MBL) in CG pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the involvement of MBL insufficiency in the pathogenesis of pediatric chronic gastritis.
- To compare MBL-2 gene mutations and serum concentrations in children with and without H. pylori infection.
Main Methods:
- Collected blood samples from 78 pediatric CG patients (H. pylori positive), 41 CG patients (H. pylori negative), and 77 controls.
- Analyzed mbl-2 gene mutations and serum MBL protein concentrations.
- Examined mbl-2 gene expression in gastric biopsies.
Main Results:
- No significant differences in mbl-2 gene mutations or serum MBL concentrations were found between CG groups and controls.
- mbl-2 gene expression was detected in gastric biopsies of CG patients.
- Gene expression was stronger in H. pylori-infected children.
Conclusions:
- MBL deficit/dysfunction is unlikely to be a risk factor for pediatric CG, with or without H. pylori.
- MBL's opsonic effect and the lectin complement pathway may represent host defense mechanisms in gastric patients.
Abstract:
The involvement of mannan-binding lectin (MBL) insufficiency in the pathogenesis of chronic gastritis (CG) in children was investigated. Blood samples were collected from 78 paediatric patients suffering from CG associated with Helicobacter pylori infection (group Hp(+)) and from 41 with the disease not associated with such an infection (group Hp(-)). Control group consisted of 77 children. The frequency of mbl-2 gene mutations and serum protein concentrations did not differ significantly in both groups as compared with controls. An expression of mbl-2 gene in gastric biopsies of CG patients was demonstrated. It was found to be stronger in H. pylori-infected children. The results presented in this paper suggest that MBL deficit/dysfunction probably does not contribute to an increased risk of CG (both associated and not associated with H. pylori infection) in children. However, MBL opsonic effect and/or the lectin pathway of complement activation may be taken into account as possible host defence mechanisms in gastric patients.
Related Concept Videos
Gastritis II: Pathophysiology
Selectins
Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Proteoglycans

