Dynamics of Helicobacter pylori colonization in relation to the host response

Abstract

The dynamics of Helicobacter pylori colonization from its acquisition through the development of steadystate are examined through a mathematical model that includes the host response. The model encompasses both host and microbiological variation. The individual capacity of the host response is shown to be a key model parameter, leading to either transient or persistent colonization, whereas the growth rate of that response has little effect. Analyses of competing strains indicate that each must occupy a specific niche, otherwise exclusion occurs. The model implies that there exists a lower bound on the host response to the indigenous microflora that is consistent with current biological views of H. pylori. Parallel models may be useful in understanding other persistent host-microbial interactions.

Helicobacter pylori genetic diversity and risk of human disease

“…We infer that H. pylori may be nourished by exudate from host tissue, rather than directly by what we eat and drink (14,15). If this view is correct, then H. pylori may need to induce host tissue injury to survive.…”

“…However, hypervirulence (excessive tissue damage) could result in more severe gastritis, atrophy, and hypochlorhydria, which permits overgrowth of more pH-sensitive competing bacterial species, and loss of habitat by replacement of gastric-type by intestinaltype epithelia (intestinal metaplasia), a tissue type that H. pylori cannot colonize. Hence, H. pylori may walk a tightrope -needing to induce sufficient response to permit nutrient release and regulation of habitat, but not so much as to result in loss of its niche (14,15). Such a coevolution model predicts that H. pylori benefits its human hosts, and indeed, these bacteria produce antibacterial substances (16) and may help suppress more virulent species.…”

“…A concept that is emerging is that they are more interactive with the host (39) and live in a different equilibrium than do cag -strains (15). For example, both in vivo and in vitro, cag + cells induce higher levels of the proinflammatory cytokines IL-1β and IL-8.…”

Helicobacter pylori adherence to gastric epithelial cells: a role for non-adhesin virulence genes

“…The bacterium colonises the gastric mucosa by adhering to and penetrating the mucus layer lining the gastric epithelium [2]. Colonisation of the gastric mucous layer protects the bacteria from the extreme acidity of the gastric lumen and displacement from the stomach by forces such as those generated by peristalsis and gastric emptying.…”

Understanding Microbe-Induced Cancers

“…Important frontiers for intervention after exposure and infection involve ways of influencing the course of an infection toward transience rather than permanence (65). If this approach is not successful, then diminishing microbial load and/or directing host responses down less oncogenic pathways would be desirable.…”