These authors equally contributed to the work.
Helicobacter pylori-derived neutrophil-activating protein increases the lifespan of monocytes and neutrophils
Article first published online: 11 JAN 2010
© 2010 Blackwell Publishing Ltd
Volume 12, Issue 6, pages 754–764, June 2010
How to Cite
Cappon, A., Babolin, C., Segat, D., Cancian, L., Amedei, A., Calzetti, F., Cassatella, M. A., D'Elios, M. M. and de Bernard, M. (2010), Helicobacter pylori-derived neutrophil-activating protein increases the lifespan of monocytes and neutrophils. Cellular Microbiology, 12: 754–764. doi: 10.1111/j.1462-5822.2010.01431.x
- Issue published online: 5 MAY 2010
- Article first published online: 11 JAN 2010
- Received 19 August, 2009; revised 20 December, 2009; accepted 21 December, 2009.
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.