The products of Helicobacter pylori that induce inflammation

Abstract

Outer membrane of Helicobacter pylori The bacterium H. pylori is known to cause chronic gastric and duodenal infection. As a result of H. pylori colonization, there is an inflammatory response in the gastric mucosa and the host produces a range of immunological mediators in an attempt to eliminate the organism. Despite this, in many cases the bacterium persists, suggesting that the outer membrane of H. pylori may have evolved to minimize the immunological response and ensure survival of the organism in the gastric environment Lipid A component In common with other bacterial species, the lipid A component of H. pylori lipopolysaccharide in the outer membrane endows the molecule with a range of immunological properties, but there are major structural differences between the lipid A of different species. H. pylori lipid A has an unusual phosphorylation and fatty acid substitution pattern which appears to translate into biological differences, since H. pylorilipid A has been shown to have lower immunological activity than that of some other species. H. pylori cell surface proteins, however, are potent inducers of the inflammatory mediators. Balance in host's inflammatory response There appears to be a balance between minimizing the host's inflammatory response to protect the bacterium and stimulating the inflammatory response, which results in chronic infection in the host Neutrophil infiltration, a characteristic of H. pylori infection, and neutrophil migration across the endothelium, is a result of the unique regulation of adhesion molecules on these cells by the bacterium.