Determination of the Frequency of Le<sup>a</sup> Antigens, Le<sup>b</sup> and Anti-Le Antibodies in Individuals Infected or not by Helicobacter Pylori

Research Article

J Bacteriol Mycol. 2018; 5(4): 1073.

Determination of the Frequency of Lea Antigens, Leb and Anti-Le Antibodies in Individuals Infected or not by Helicobacter Pylori

Rampelotti JC, Bueno EC, Valcarenghi D and Geraldo A*

University of Vale do Itajaí, Brazil

*Corresponding author: Alexandre Geraldo, University of Vale do Itajaí, Uruguai Street, Brazil; Email: [email protected]

Received: June 01, 2018; Accepted: July 03, 2018; Published: July 10, 2018


Introduction: Helicobacter pylori, has an affinity for the gastric mucosa, and may be associated with blood group systems, among them the Lewis System. The adhesins are one of the virulence factors of H. pylori and studies have indicated as receptors for adhesins certain blood group antigens. Therefore, the objective of this study was to determine the frequency of Lea antigens, Leb antigens and anti-Lex antibodies in individuals infected or not with H. pylori.

Methods: Samples were subjected to phenotype for Lea and Leb antigens and serological tests for determination of H. pylori using IgA / IgG / IgM class antibodies.

Results: Of the 88 individuals surveyed, 18% had Lea antigen, 74% Leb and 8% did not present Lea and Leb antigens in the erythrocytes studied. 54% of the students who had active H. pylori infection expressed the erbocytic Leb antigen.

Discussion: The Le (a-b+) phenotype was the most prevalent with 74%. Individuals who reported having no symptoms had a higher percentage of active infection by H. pylori, with 17%, and were carriers of the Le (a-b+) phenotype.

Conclusion: The group with the highest frequency of active H. pylori infection was the Le (a-b+) phenotype, and this antigen could also be associated with the Leb antigen isomers, thus serving as a receptor for H. pylori in the tissue. In this way, drugs may be developed with a mechanism to prevent the binding of H. pylori to the Lewis System antigens in the gastric cavity during treatment, preventing infection.

Keywords: Lewis Blood Group System; Helicobacter Pylori; Gastritis; Peptic Ulcer; Antigens


In the 1970s and 1980s, researchers used silver staining to evaluate biopsies of peptic ulcers and identified curved bacteria that colonized the gastric antrum of hosts. Thus, it was possible to describe the microbiological properties of these bacteria, which were called Campylobacter pylori, which later became known as Helicobacter pylori (H. pylori) [1].

The genus Helicobacter was defined by studies of the composition of ribosomal RNA [2], sequencing and hybridization of the DNA of the bacterium [3]. This genus, along with others (Campylobacter, Arcobacter and Wolinella), constitutes the superfamily VI of gramnegative bacteria [4].

The morphology of H. pylori, observed under optical and electronic microscopy, is homogeneous, presenting a curved or spiral structure, with a smooth surface and rounded, mobile, non-spore and microaerophilic ends. It measures approximately 0.5μm to 1μm in width and 3μm in length, having four to six sheathed unipolar flagellae and terminal bulbs at the smooth ends [5]. The oral-oral, gastrooral and fecal-oral transmission are the most probable among other possibilities, such as the one that suggests that the drinking water is vehicle of the bacterium. This bacterium synthesizes urease, which generates ammonia, damaging the gastric mucosa, since ammonia neutralizes the acidic pH of the stomach, allowing the body to live in the gastric mucosa [6]. It is estimated that about 50% of the world population is infected with H. pylori, and this prevalence is higher in developing countries [7]. In Brazil, the prevalence of H. pylori has been reported among adults and children at rates ranging from 34% to 80% [7-10]. Population studies in regions with poor living conditions have shown that, in general, prevalence rates are characterized by a rapid increase with age from the onset of childhood, reaching a plateau around 80% after 20 years of age [11-13].

Another important point is the zoonotic transmission of the genus Helicobacter, due to the presence of gastric microorganisms with similar morphology in the stomach of several animal species (dogs, cats, pigs, cattle, sheep, birds, ferrets, Guinea pigs, monkeys, mice, hamsters, marmots, foxes, cheetahs, dolphins, beluga whales and others). For this reason domestic animals have been frequently reported as potential sources of Helicobacter spp infection [14].

In the literature there are few epidemiological studies of genetic predisposition for gastric diseases. However, previous studies have shown an association of antigens of Lewis and ABH blood groups with susceptibility to H. pylori colonization [15,16].

The Lewis Blood Group System was discovered in 1946 after the identification of the antigen Le ant antigen in children with fetal and neonatal hemolytic disease (DHFRN). Years later, in 1949, researchers demonstrated the presence of Lewis antigens in saliva and plasma. Thereafter, they demonstrate the loss of these Lewis antigens in vivo. This system is currently composed of six glycolipid and glycoprotein antigens, present in saliva, tear, urine, gastric juices, epithelial tissues, bone marrow, kidneys, lymphocytes, platelets, pancreas, adrenals and skeletal muscle [17].

Among blood groups, Lewis antigens are the only ones not to be synthesized by erythrocytes. They are produced by tissue cells and secreted in organic liquids, and their antigens are mainly found in secretions and plasma [18].

Expression of the Lewis antigens depends on the inherited alleles at two independent locus (secretor [SE] gene) FUT2 and (Lewis [LE] gene) FUT3. These alleles encode separate fucosyltransferases that interact to form Lewis antigens in secretions and fluids. The formation of these antigens occurs through the adsorption of carbohydrates from the plasma. These antigens are widely distributed in human and fluid tissues [15]. The FUT3 enzyme acts on the phenotypic expression of the Lewis System by fucosylation of precursor oligosaccharides (OP) type 1 (Galactose-β1 → 3N-acetylglucosamine-β1-R) and type 2 (Galactose-β1 → 4N-acetylglucosamine-β1 -R). These precursors have a free and non-reduced terminal end to which fucose molecules can be added, and an opposite one, which can be attached to carbohydrates, lipids or proteins [16,19,20,21]. Fucosyltransferase Lewis adds a fucose molecule to the carbon-2 of N-acetyl glucosamine (NacGlu) to generate the Le ant antigen (Galactose-a1 → 3 [Fucose-a1 → 2] N-acetyl glucosamine-R). The secretory fucosyltransferase adds a fucose molecule to the carbon 2 of the terminal galactose of the precursor oligosaccharide, giving rise to H-type 1 antigen (Fucose-a1 → 2Galactose-a1 → 3N-acetylglucosamine-R). Fucosyltransferase Lewis adds another fucose molecule to the carbon-2 of N-acetyl glucosamine, generating the antigen Leb (Fucose-a1 → 2Galactose-a1 → 3 [Fucose-a1 → 2] N-acetyl glucosamine-R) [21]. Therefore, the Le ant antigen has epitopes that may be present in type 1 H, which may cross-react with anti-Lea and anti-H antibodies (Figure 1) [22].