Helicobacter pylori – interactions with phagocytes

Helicobacter pylori possess the remarkable ability to persist in the human stomach for long periods, probably for life. For such prolonged colonization this pathogen must have acquired sophisticated mechanisms allowing it to escape both innate and acquired cellular immunity. The most important accessory cells directly involved in the eradication of bacteria are phagocytic cells of the monocytic and myelocytic lineages and, in particular, the macrophages and polymorphonuclear neutrophils. Bacteria which are directly recognized, ingested and destroyed by phagocytes are not pathogenic in immunocompetent individuals. In contrast, some bacterial pathogens have evolved various mechanisms allowing them to resist direct engulfment by phagocytes. These pathogens usually exploit easily attainable host constituents which are pivotal in physiological functions. H. pylori express numerous surface ligands: sialic acid-specific haemagglutinins1, heparan sulphate-binding proteins2, extracellular matrix-binding compounds3, Lewis X and Lewis Y determinants4–6, which interact with specific receptors on various host cells including phagocytes. In this study we try to establish the role of those ligand—receptor interactions in the engulfment of H. pylori reference and clinical strains by phagocytes.