Helicobacter pylori is a spiral-shaped, flagellated, microaerophilic Gram-negative bacterium that colonizes the gastric epithelium of humans. All persons infected with H. pylori have gastritis, and some will develop severe disease such as peptic ulcers or gastric cancer. A characteristic feature of this infection is the pronounced accumulation of phagocytes, particularly neutrophils, in the gastric mucosa. H. pylori thrives in a phagocyte-rich environment, and we describe here how this organism uses an array of novel virulence factors to manipulate chemotaxis, phagocytosis, membrane trafficking and the respiratory burst as a means to evade elimination by the innate immune response.