Helicobacter pylori-derived neutrophil-activating protein increases the lifespan of monocytes and neutrophils.
Cell Microbiol. 2010 Jun; 12(6):754-64
This interesting article describes a novel role for a Helicobacter pylori protein in modulating the inflammatory process.
The paper shows that neutrophil-activating protein (HP-NAP) is able to induce survival of monocytes, via an IL-1beta-dependent process. Monocytes exposed to HP-NAP secrete IL-1beta that can then induce survival in naive monocytes. However, it is likely that other factors may be involved, since inhibition of IL-1beta did not completely block the effect. HP-NAP was also shown to activate some anti-apoptotic proteins, particularly the anti-apoptotic protein A1, though its not clear whether this is dependent on IL-1beta. Finally, they indirectly demonstrated that HP-NAP is able to induce survival in neutrophils but only in the presence of monocytes. This interesting observation suggests that monocytes may work as intermediates in the stimulation of other innate immune response cells. Whether contaminating monocytes have mediated the reported effect on neutrophil activation in previous studies is unclear and deserves further study.
Steele-Mortimer O and Ibarra J: F1000Prime Recommendation of [Cappon A et al., Cell Microbiol 2010, 12(6):754-64]. In F1000Prime, 21 Jul 2010; DOI: 10.3410/f.4215956.4005054. F1000Prime.com/4215956#eval4005054
F1000Prime Recommendations, Dissents and Comments for [Cappon A et al., Cell Microbiol 2010, 12(6):754-64]. In F1000Prime, 07 Dec 2013; F1000Prime.com/4215956
PLoS Pathog. 2013 Feb; 9(2):e1003189
J Infect Dis. 2005 Sep 1; 192(5):783-90
PLoS Pathog. 2006 Sep; 2(9):e97
J Clin Invest. 2012 Mar 1; 122(3):1082-96
J Exp Med. 2008 May 12; 205(5):1155-71
Nat Med. 2008 Jul; 14(7):738-47
Cell Host Microbe. 2008 Aug 14; 4(2):170-8
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-1beta, 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.
has been added to your "Faculty I'm Following" page in MyF1000
Follow/Unfollow any Faculty via their recommendations, biography pages, or MyF1000
If you've forgotten your password, please enter your email address below and we'll send you instructions on how to reset your password.
The email address should be the one you originally registered with F1000.
You registered with F1000 via Google, so we cannot reset your password.
To sign in, please click here.
If you still need help with your Google account password, please click here.
You registered with F1000 via Facebook, so we cannot reset your password.
To sign in, please click here.
If you still need help with your Facebook account password, please click here.
We have sent an email to , please follow the instructions to reset your password.
If you don't receive this email, please check your spam filters and/or contact email@example.com.