Helicobacter pylori‐derived neutrophil‐activating protein increases the lifespan of monocytes and neutrophils |
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| Authors: | Andrea Cappon Chiara Babolin Daniela Segat Laila Cancian Amedeo Amedei Federica Calzetti Marco A Cassatella Mario M D'Elios Marina de Bernard |
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| Institution: | 1. Venetian Institute of Molecular Medicine, Padua, Italy.;2. These authors equally contributed to the work.;3. Department of Biomedical Sciences, University of Padua, Padua, Italy.;4. Department of Virology, Faculty of Medicine, Imperial College London Imperial College, London, UK.;5. Department of Internal Medicine, University of Florence, Florence, Italy.;6. Department of Biomedicine, Azienda Ospedaliera Universitaria Careggi, Florence, Italy.;7. Department of Pathology, Division of General Pathology, University of Verona, Verona, Italy.;8. Department of Biology, University of Padua, Padua, Italy. |
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| Abstract: | An invariable feature of Helicobacter pylori‐infected gastric mucosa is the persistent infiltration of inflammatory cells. The neutrophil‐activating protein (HP‐NAP) has a pivotal role in triggering and orchestrating the phlogistic process associated with H. pylori infection. Aim of this study was to address whether HP‐NAP might further contribute to the inflammation by increasing the lifespan of inflammatory cells. We report that HP‐NAP is able to prolong the lifespan of monocytes, in parallel with the induction of the anti‐apoptotic proteins A1, Mcl‐1, Bcl‐2 and Bcl‐XL. This effect does not result from a direct action on the apoptotic machinery, but rather it requires the release of endogenous pro‐survival factors, such as interleukin‐1β, which probably acts in synergy with other unidentified mediators. We also report that HP‐NAP promotes the survival of Ficoll‐purified neutrophils in a monocyte‐dependent fashion: indeed, mononuclear cell depletion of Ficoll‐purified neutrophils completely abolished the pro‐survival effect by HP‐NAP. In conclusion, our data reinforce the notion that HP‐NAP has a pivotal role in sustaining a prolonged activation of myeloid cells. |
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