What is an alternative hypothesis of the pathophysiology of Helicobacter pylori (H pylori) infection?

Updated: Jul 21, 2021
  • Author: Luigi Santacroce, MD; Chief Editor: BS Anand, MD  more...
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Another hypothesis states that H pylori may recall immune cells from afar because of its own molecules, such as urea or lipopolysaccharide (LPS). Outer-membrane permeability is a function mediated by LPS. Despite the presence of bacterial LPS in biologically active quantities in the gastric mucosa, the mechanisms by which it may recall the immune cells are still unknown. According to one hypothesis, H pylori may induce the production of autoantibodies against the host's gastric lining.

The LPS of H pylori shows certain blood group antigens, such as Leb, Lex, Ley, and H-type I. Such antigens are thought to represent important virulence factors involved in the adhesive process of the germ. Leb constitutes an adhesin, and differences exist in the Le compositions of adherent and nonadherent bacteria. This, perhaps, accounts for a relationship between adhesion and Le expression. Hage and colleagues identified the BabA protein (Blood group antigen-binding Adhesin) in H pylori that interacts with gastric mucus binding Leb antigens, confirming the relationship. [5] As a consequence, H+ bridges may be formed, strongly anchoring the bacterium to the gastric mucosa.

In addition, any Le antigen shows phase variation leading to the spontaneous and random switching on and off of the expression of these antigens. For example, the H-type I antigen seems to be the result of a reversible singular nucleotidic deletion/insertion in a tract of a glycosyl transferase gene. The LPS of the H pylori also seems to influence tumoral proliferation of ECL cells, stimulating the intracellular polyamine biosynthesis pathway and ornithine decarboxylase activity by the activation of a CD14 receptor on the ECL cell.

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