Histo-Blood Group Carbohydrates and Helicobacter pylori Infection

Abstract

b , ALe b , BLe b ). Therefore, individuals carrying both FUTII and FUTIII enzymes are classified as Secretors. Non Secretors did not carry the FUTII being unable to synthesize these carbohydrate antigens but when carrying the FUTIII enzyme they express high levels of Le a an- tigen (2). These biochemical events affect the susceptibility and resist - ance to microorganisms like H. pylori. Th e experimental demonstration that the Le b glycolipd acts as an important receptor for H. pylori (3) and the subsequent characteriza- tion of its BabA adhesin (Blood group antigen binding Adhesin) (4) filled a gap opened with the old report that individuals belonging to O blood group are more prone to suffer from peptic ulcers (5). These stud - ies clearly established a functional relationship between histo-blood group carbohydrates and a microorganism infecting thousands of peo- ple around the globe. It reached its peak with the observation that H. pylori strains isolated from Amerindians are strongly adapted to infect those belonging to O blood group. This adaptability is coincident with the high prevalence of blood group O in South America natives (6). by CagA strains is strongly associated with this blood group, especially in adult patients with chronic active gastritis and peptic ulcers (9,10). Recently it was shown that the Secretor phenotype plays an im- portant role in intrinsic resistance to infection by this organism. The high concentration of mucus in carriers of this phenotype appears to be crucial in preventing the adhesion of BabA strains to histo-blood group carbohydrates expressed in the gastrointestinal tract. Addition- ally, carriers of the weak secretor phenotype (weak secretor) have par- tial protection against mucosal inflammation and proliferation of this microorganism, thus confirming the importance of the FUT2 gene in resistance to infection by some H. pylori strains (11). Although most studies show that the presence of Le b carbohydrate increase the susceptibility of O blood group for infection by H. pylori some questions concerning the contribution of histo-blood group car- bohydrates still need to be answered. Carries of chronic gastritis, peptic ulcer and gastric cancer did not present necessarily evidence of infec- tion by this microorganism. Are these carbohydrates acting only as lig- ands for H. pylori adhesion or playing additional roles in the manifesta- tion of these diseases? The gastric cancer related to H. pylori is more frequent in A blood group. What is the influence of histo-blood group carbohydrates in this differential susceptibility when compared with O blood groups? The presence of FUTII glycosyltransferase diversifies and reduces the extension of histo-blood group carbohydrate chains. What is the contribution of these short hito-blood group carbohydrate chains in infection by this organism? Understanding the biological and clinical importance of histo- blood group carbohydrates in the diseases resulting from H. pylori in- fection may provide a better basis for potential therapeutic applications. Would be possible to identify adhesins other than BabA and use them in the production of vaccines capable of inducing localized humoral immune responses with the expression of high affinity specific IgA anti- bodies. Moreover, these carbohydrates could be useful in anti-adhesion therapy which apart from deterring colonization by this microorgan- ism may contribute to the treatment of infection by strains resistant to conventional antibiotics (1). Studies aimed to clarify the relationships between histo-blood group carbohydrates and H. pylori may contribute to understanding the selective forces that created and maintain the high polymorphism of ABO, Secretor and Lewis histo-blood group carbohydrates in man.