Helicobacter pylori inhibits phagocytosis by professional phagocytes involving type IV secretion components

Gastric infections by Helicobacter pylori are characteristically associated with an intense inflammation and infiltration of mainly polymorphonuclear lymphocytes (PMNs) and monocytes. The inflammatory response by infiltrated immune cells appears to be a primary cause of the damage to surface epithel ial layers and may eventually result in gastritis, peptic ulcer, gastric ca ncer and/or MALT-associated gastric lymphoma. Our analysis of the interacti on between H. pylori and PMNs and monocytes revealed that H. pylori inhibit s its own uptake by these professional phagocytes. To some degree, this eff ect resembles antiphagocytosis by Yersinia enterocolitica. Increasing numbe rs of bacteria associated per cell are more efficient at blocking their own engulfment. In H. pylori, bacterial protein synthesis is necessary to bloc k phagocytic uptake, as shown by the time and concentration dependence of t he bacteriostatic protein synthesis inhibitor chloramphenicol. Furthermore, H. pylori appears broadly to inhibit the phagocytic function of monocytes and PMNs, as infection with H. pylori abrogates the phagocytes' ability to engulf latex beads or adherent Neisseria gonorrhoeae cells. This antiphagoc ytic phenotype depends on distinct virulence (vir) genes, such as virB7 and virB11, encoding core components of a putative type IV secretion apparatus . Our data indicate that H. pylori exhibits an antiphagocytic activity that may play an essential role in the immune escape of this persistent pathoge n.