Studies on the interaction of Helicobacter pylori with extracellular matrix proteins

Abstract

Helicobacter pylori is a common human pathogen that persistently colonises the stomach of half the worlds population. The majority of people infected with H. pylori are asymptomatic, however, a proportion develop severe gastro-duodenal pathologies including gastritis, gastric/duodenal ulcers and gastric cancers. H. pylori has also been associated with other diseases such as iron-deficiency anaemia and autoimmune gastritis. H. pylori membrane proteins, such as adhesins BabA and AlpA, play an important role in the successful invasion and colonisation of host gastric mucosa. Damage to the gastric mucosa caused by the inflammatory response to H. pylori infection as well as microlesions caused by some foods exposes the extracellular matrix (ECM) to further sites of attachment for H. pylori. Indeed, numerous studies have shown that H. pylori can interact and associate with ECM ligands, including laminin, but few receptors to these ligands have been identified to date. An important host defence mechanism against infecting pathogens is to create a low iron environment. Iron is an essential micronutrient and its acquisition from the environment is critical for bacterial survival. However, pathogenic bacteria have evolved mechanisms to adapt to and acquire iron from the host, thereby, avoiding clearance.