Inflammation provides one such interaction, and so I have proposed that H. pylori might trigger inflammation for the purpose of acquiring nutrients. An apparent paradox in H. pylori biology is that although the organisms do not invade the gastric tissue, they can cause irritation there. Rather, as we and others have found, the microbes release chemicals that the stomach tissue absorbs. These compounds attract phagocytic cells, such as leukocytes and macrophages, that induce gastritis. The host is not entirely passive while H. pylori bombard it with noxious substances.
Humans mount an immune response, primarily by making antibodies to the microbe.
This response apparently does not function well, though, because the infection and the antibodies almost inevitably coexist for decades. I believe the choice was made long ago in favor of tolerance. Fortunately, it is not in H. pylori's best interest to take advantage of this passivity, growing to overwhelming numbers and ultimately killing its host. First, doing so would limit the infection's opportunity to spread. And third, further growth might exhaust the mechanisms keeping the immune system in check, leading to severe inflammation, atrophic gastritis and, eventually, a loss of gastric acidity.