Amedeo Amedei, Andrea Cappon, Gaia Codolo, Anna Cabrelle, Alessandra Polenghi, Marisa Benagiano, Elisabetta Tasca, Annalisa Azzurri, Mario Milco D’Elios, Gianfranco Del Prete, Marina de Bernard
J Clin Invest.
2006;
116(4):1092–1101
doi:10.1172/JCI27177
This article Copyright © 2006, The American Society for Clinical Investigation
Abstract
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T
he Helicobacter pylori neutrophil-activating protein (HP-NAP) is a virulence factor of H. pylori that stimulates in neutrophils high production of oxygen radicals and adhesion to endothelial cells. We report here that HP-NAP is a TLR2 agonist able to induce the expression of IL-12 and IL-23 by neutrophils and monocytes. Addition in culture of HP-NAP, as an immune modulator, to antigen-induced T cell lines resulted in a remarkable increase in the number of IFN-γ–producing T cells and decrease of IL-4–secreting cells, thus shifting the cytokine profile of antigen-activated human T cells from Th2 to a Th1 cytotoxic phenotype. We also found that in vivo HP-NAP elicited an antigen-specific Th1-polarized T cell response in the gastric mucosa of H. pylori–infected patients. These data indicate HP-NAP as an important factor of H. pylori able to elicit cells of the innate immune system to produce IL-12 and IL-23, and they suggest it as a new tool for promoting Th1 immune responses.
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