Hp(2-20) peptide of Helicobacter pylori and the innate immune receptors: specific role(s) of the formyl peptide receptors.

Helicobacter pylori (H. pylori) is a microaerophilic, Gram-negative bacterium that affects more than half of the world's population. H. pylori has co-evolved with humans to be transmitted from person to person and to persistently colonize the stomach. A well-choreographed equilibrium between bacterial effectors and host responses permits microbial persistence and health of the host but confers risk of serious diseases. During its long coexistence with humans, H. pylori has evolved complex strategies to limit the degree and extent of gastric mucosal damage and inflammation as well as immune effector activity. In this complex strategy an important role is played by the interaction of H. pylori with a specific class of innate immune receptors, named N-formyl peptide receptor family (FPRs). In the last years several virulence factors have been studied in an effort to correlate bacterial phenotype with specific gastric manifestations and to clarify the pathogenetic mechanisms. Several peptides produced by H. pylori appear to be involved in inflammation associated with the infection. A particular interest has been focused on the Hp(2-20) peptide derived from the bacteria. Thus, aim of the article is to comment on some advances in the elucidation of specific interactions between the Hp(2-20) peptide and FPRs.