Helicobacter pylori are bacteria that have coevolved with humans to be transmitted from person to person and to persistently colonize the stomach. Their population structure is a model for the ecology of the indigenous microbiota. A well-choreographed equilibrium between bacterial effectors and host responses permits microbial persistence and health of the host but confers risk of serious diseases, including peptic ulceration and gastric neoplasia.

The twin hallmarks of the interaction between Helicobacter pylori and humans are its persistence during the life of the host, and the host’s responses to its continuing presence. This conflict appears paradoxical, but both the microbes and the host adapt to the other in the form of a long-standing dynamic equilibrium (1, S1 [http://www. jci. org/cgi/content/full/113/3/321/DC1]). Our understanding of the phenomena underlying these interactions is growing. The relationships are important, both because of the major role of H. pylori in promoting risk of peptic ulcer disease (2) and non-cardia adenocarcinoma of the stomach (3), and because of the emerging evidence that gastric H. pylori colonization has a protective role in relation to severe gastro-esophageal reflux disease and its sequelae, Barrett esophagus and adenocarcinoma of the esophagus (reviewed in ref. 4). New studies suggest other important impacts of H. pylori colonization on human physiology (5, 6).