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Updated: Jun 21, 2026

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
Published on: January 7, 2019
[Mannan-binding lectin (MBL) in duodenal ulcer and gastritis]
Leokadia Bak-Romaniszyn1, Anna Swierzko, Janusz Szemraj
1Department of Nutrition in Digestive Tract Diseases, Medical University of Łódź. kpg@iczmp.edu.pl
Unlabelled:
H. pylori is considered to be a major etiological agent of chronic gastritis. Mannan-binding lectin (MBL) is one of the key factors of the innate immunity. It belongs to collectins binding to saccharides on the surface of a variety of pathogenic microorganisms, H. pylori including. MBL after coating the bacteria is recognized by the receptor on macrophages, facilitates phagocytosis by direct opsonization and activates complement via the lectin pathway which protects the host against infection. Single nucleotide polymorphisms of MBL2 gene affect both MBL concentration and biological activity.
Aim:
Evaluation of the correlation between the occurrence of MBL2 gene mutations, MBL concentration in serum, and prevalence of duodenal ulcer and chronic gastritis with or without H. pylori infection.
Material And Methods:
The study comprised 174 children aged 6-17 years (mean 13.1 x 4.2), among them 74 children with H. pylori infection-associated chronic gastritis (group Hp+), 41 with H. pylori infection excluded (group Hp-), and 11 children with duodenal ulcer (DU). The control group consisted of 46 healthy children without gastritis, endoscopically checked. Determination of serum MBL concentration was performed using ELISA. Polymorphisms of the promoter region as well as mutations of exon 1 MBL2 gene were identified with polymerase chain reaction methods. H. pylori was detected with both urease test and histopathology Giemsa staining.
Results:
MBL serum concentration was significantly lower in children with both Hp+ (1809 ng/ml) and Hp-gastritis (1439 ng/ml) when compared to the control group (2545 ng/ml) (p < 0.05 and p < 0.01, respectively). The same trend (however the difference was insignificant) was observed in the case of DU group (1643 ng/ml). The frequency of MBL2 gene mutations did not differ between any group of patients as compared to controls.
Conclusions:
No influence of MBL2 genotype on the incidence of duodenal ulcer or gastritis was found. MBL serum concentrations are lower in chronic gastritis patients (with or without H. pylori infection) when compared to the age-matched healthy individuals.
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