The neutrophil-activating protein of Helicobacter pylori promotes Th1 immune responses |
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Authors: | Amedei Amedeo Cappon Andrea Codolo Gaia Cabrelle Anna Polenghi Alessandra Benagiano Marisa Tasca Elisabetta Azzurri Annalisa D'Elios Mario Milco Del Prete Gianfranco de Bernard Marina |
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Affiliation: | Department of Internal Medicine, University of Florence, Florence, Italy. |
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Abstract: | The 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-gamma-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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