Helicobacter pylori Pathogen-Associated Molecular Patterns: Friends or Foes?

Abstract

Microbial infections are sensed by the host immune system by recognizing signature molecules called Pathogen-Associated Molecular Patterns-PAMPs. The binding of these biomolecules to innate immune receptors, called Pattern Recognition Receptors (PRRs), alerts the host cell, activating microbicidal and pro-inflammatory responses. The outcome of the inflammatory cascade depends on the subtle balance between the bacterial burn and the host immune response. The role of PRRs is to promote the clearance of the pathogen and to limit the infection by bumping inflammatory response. However, many bacteria, including Helicobacter pylori, evolved to escape PRRs' recognition through different camouflages in their molecular pattern. This review examines all the different types of H. pylori PAMPs, their roles during the infection, and the mechanisms they evolved to escape the host recognition.

Keywords: ADP-heptose; LPS; OMV; PAMP.

Figure 1

H. pylori survival strategies against phagocytes. The bacterium secretes catalase and SOD to reduce ROS toxicity, synthetizes arginase to limit NO production, reduces host NADPH oxidase response, and induces macrophage apoptosis.

Figure 2

H. pylori LPS structure. Lacking the canonical inner and outer core organization, H. pylori LPS shows a short core and a longer O-antigen with a terminal Lewis antigen.

Figure 3

Schematic release and action of H. pylori heptose metabolites. HBP and ADP-heptose enter epithelial cells to induce TIFAsome formation and NF-kB activation.