Open AccessHelicobacter pylori ‐derived neutrophil‐activating protein increases the lifespan of monocytes and neutrophils
Author(s) -
Cappon Andrea,
Babolin Chiara,
Segat Daniela,
Cancian Laila,
Amedei Amedeo,
Calzetti Federica,
Cassatella Marco A.,
D'Elios Mario M.,
de Bernard Marina
Publication year - 2010
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2010.01431.x
Subject(s) - helicobacter pylori , nap , biology , inflammation , immunology , monocyte , apoptosis , myeloid , interleukin 8 , ficoll , peripheral blood mononuclear cell , in vitro , genetics , neuroscience
Summary 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‐X L . 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.