We are only beginning to understand the complex mechanisms used by H. pylori to establish infection and to maintain colonization in the same host over a period of many years. Penetration of the mucous layer likely involves motility, phospholipase activity, and mucinase activity. H. pylori-mediated reduction of mucus synthesis or secretion may also assist the bacterium in gaining access to the epithelium and persisting at this location. Adherence allows the bacteria to anchor themselves to the epithelial layer, but bacteria that remain attached to epithelial cells will eventually be swept away as these cells die and are exfoliated. Thus, a proportion of the H. pylori population exists in the nonadherent state. H. pylori must also contend with antibodies and phagocytic cells as the host mounts an immune response.
Colonization by H. pylori has only been confirmed in the gastric mucosa. Limitation to this site could be due to competition by other organisms in the mouth and small intestine. Other Helicobacter spp. have been isolated from blood and deep tissues, but H. pylori has not. Perhaps the exquisite sensitivity of H. pylori to complement-mediated lysis (261, 265) renders it incapable of causing extragastric disease; however, circumstantial evidence suggests that H. pylori may be present in the liver (233, 259).
Preventing the establishment of long-term colonization, or even curing an established H. pylori infection, may be achieved either by killing all organisms or by antagonizing one or more of the persistence mechanisms and suppressing growth until the combination of host immune response, exfoliation, and movement of gastric contents purge the last bacterium from the stomach. Data in humans on prevention of colonization or spontaneous cure are sparse; however, there is some evidence for both phenomena (29, 115, 198, 202, 328, 372). Widespread treatment of H. pylori infection with multidrug regimens is problematic even in industrialized nations. Thus, until an effective vaccine is developed to prevent H. pylori infection, improved sanitation and public education may be the most practical means of limiting infection.
At present, dissecting the individual contributions of the factors discussed in this chapter is exceedingly difficult. The development of new research tools, such as the completed genome sequence and superior in vivo and in vitro models will no doubt facilitate future studies of H. pylori adherence and colonization.
Copyright © 2001, ASM Press.