Mannose-binding lectin serum levels and (Gly54asp) gene polymorphism in recurrent aphthous stomatitis: A case-control study

Abstract

Objectives: Dysregulation of the immune response appears to play a significant role in recurrent aphthous stomatitis (RAS) development. The main objective of this case–control study is to investigate the blood levels of mannose-binding lectin (MBL) and the frequency of the MBL2 gene (gly54asp) polymorphism in RAS patients, including 40 RAS patients and 40 healthy controls. Methods: Serum MBL levels were determined by ELISA, while the PCR-restriction fragment length polymorphism was used in MBL2 genotyping. Results: The median serum MBL level was significantly lower in the RAS group than in the control group (975 ng/mL (545–1320) vs. 1760 ng/mL (1254–2134); p≤ 0.001). The MBL levels were significantly lower in the BB genotype, whereas they were significantly higher in the wild type AA with a median of 525 and 1340 ng/mL, respectively ( p =0.005). The B allele was expressed in significantly higher percentages of RAS patients than in controls. There was no significant association between MBL serum levels ( p=0.685) or MBL2 codon 54 genotypes ( p=0.382) with the type of ulcers. Conclusion: There was an association between low MBL serum levels and the variant allele B of the MBL2 (gly54asp) gene, and the susceptibility to RAS. As a result, potential novel therapeutic options for RAS patients with MBL deficiency should be investigated.

Gene polymorphisms and serum levels of mannose‐binding lectin in Czech patients with recurrent aphthous stomatitis: A case–control study

“…The MBL2 gene variability has very recently been identified as a susceptibility factor for RAS in the Egyptian population. The authors investigated 40 healthy controls and 40 patients with RAS and found that the B allele of the MBL2 gene at codon 54 was significantly associated with the lowest serum MBL level and RAS development 2 . This is not consistent with our results in the Czech population: in this study, we observed no association of any of the six MBL2 gene polymorphisms (rs11003125, rs7096206, rs7095891, rs5030737, rs1800450, rs1800451) alleles, genotypes, haplotypes and haplogenotypes with RAS.…”

“…Similarly, Inanc and colleagues reported no significant differences in MBL levels between RAS patients and healthy controls. 28 In contrast, in the recent study by Baiomy et al, 2 the median serum MBL level was significantly lower in a group of patients with RAS compared to control subjects. These authors also found that serum MBL levels varied significantly among the three different genotypes of Gly/Asp substitution in codon 54 of exon 1 MBL2 gene.…”

“…The aetiology of this disease is still controversial; however, several factors, such as trauma, microbial, nutritional, and hormonal changes, as well as the immunological constitution and genetic predisposition, have been proposed to play a role 1 . A very recent case–control study in the Egyptian population suggested that single nucleotide polymorphism (SNP) Gly54Asp (rs1800450) of the mannose‐binding lectin 2 ( MBL2 ) gene might affect the mannose‐binding lectin (MBL) serum level and RAS development 2 …”

“…1 A very recent case-control study in the Egyptian population suggested that single nucleotide polymorphism (SNP) Gly54Asp (rs1800450) of the mannose-binding lectin 2 (MBL2) gene might affect the mannose-binding lectin (MBL) serum level and RAS development. 2 The MBL is a component of the innate immune system that plays a role as a soluble pathogen recognition pattern molecule, and triggers activation of the lectin pathway of complement. 3 In addition, MBL participates in the modulation of inflammation, as it can trigger the release of pro-inflammatory cytokines.…”

“…5 The human MBL2 gene is mapped on the chromosome 10 (10q11. [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21] and contains a number of polymorphic loci (Figure 1) with possible functional implications. 6 Three polymorphisms in the promoter region of the MBL2 gene are: H/L (nucleotide À550), X/Y (nucleotide À221) and P/Q (at the +4 in the 5 0 UTR).…”