The role of persistence in Helicobacter pylori pathogenesis

Purpose of review Helicobacter pylori induces chronic gastritis and is the strongest known risk factor for peptic ulcer disease and distal gastric cancer, yet only a fraction of colonized individuals ever develop clinical disease. The aim of this article is to provide an overview of recent advances into mechanisms of H. pylori persistence and to incorporate these findings into our current understanding of H. pylori pathogenesis. Recent findings Recent studies have heightened awareness of the significance of bacterial persistence in H. pylori-associated diseases. Persistence is achieved through initial interactions between H. pylori adhesins and cellular receptors, after which H. pylori must avoid clearance by the immune system. This is accomplished by avoiding host recognition, by producing specific bacterial factors that stimulate selective expression of host genes, and by inducing an ineffective T-cell response. Further, it has become increasingly evident that the genetic diversity of H. pylori also plays a significant role in its persistence. Summary H. pylori persists in its acidic gastric niche, typically for the lifetime of the host. This persistence increases the risk of diseases such as peptic ulcer disease and gastric cancer. Delineation of mechanisms that regulate ongoing H. pylori-host interactions will not only improve targeted diagnostic and therapeutic modalities, but may also provide insights into other diseases that arise within the context of chronic pathogen infection.