Open AccessThe neutrophil‐activating protein of Helicobacter pylori (HP‐NAP) as an immune modulating agent
Author(s) -
D'Elios Mario Milco,
Amedei Amedeo,
Cappon Andrea,
Del Prete Gianfranco,
De Bernard Marina
Publication year - 2007
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2007.00258.x
Subject(s) - immune system , biology , tumor necrosis factor alpha , immunology , nap , chemokine , virulence factor , helicobacter pylori , tlr2 , inflammation , cytotoxic t cell , immunotherapy , microbiology and biotechnology , innate immune system , virulence , biochemistry , genetics , neuroscience , gene , in vitro
During evolution microorganisms have developed several immune modulating strategies. The Helicobacter pylori neutrophil‐activating protein (HP‐NAP) is a virulence factor that attracts and activates neutrophils, and promotes their endothelial adhesion and the production of oxygen radicals and chemokines, including CXCL8, CCL3 and CCL4. HP‐NAP, a TLR2 agonist, is an immune modulator able to induce the expression of interleukin‐12 (IL‐12) and IL‐23 by human neutrophils and monocytes. In fact, HP‐NAP has the potential to shift antigen‐specific T‐cell responses from a predominant Th2 to a polarized Th1 cytotoxic phenotype, characterized by high levels of interferon‐γ and tumor necrosis factor‐α production. Thus, HP‐NAP is a key factor driving Th1 inflammation in H. pylori infection and may be a new tool for future therapeutic strategies aimed at redirecting Th2 into Th1 responses, for example in atopy, vaccinology and cancer immunotherapy.