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Helicobacter pylori-derived neutrophil-activating protein increases the lifespan of monocytes and neutrophils.
Cell Microbiol. 2010 Jun; 12(6):754-64
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21 Jul 2010
Olivia Steele-Mortimer
F1000 Microbiology
Rocky Mountain Laboratories, National Institute of Allergy and Infectious Disease, NIH,
Hamilton , MT, USA.
F1000 Microbiology
Rocky Mountain Laboratories, National Institute of Allergy and Infectious Disease, NIH,
Hamilton , MT, USA.
Jose Antonio Ibarra
F1000 Microbiology
Rocky Mountain Laboratories, National Institute of Allergy and Infectious Disease, NIH,
Hamilton, MT, USA.
F1000 Microbiology
Rocky Mountain Laboratories, National Institute of Allergy and Infectious Disease, NIH,
Hamilton, MT, USA.
Interesting Hypothesis, New Finding
DOI: 10.3410/f.4215956.4005054
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...Continue reading
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...Continue reading
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 it’s 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.
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 it’s 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.
Disclosures
None declared
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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, 25 May 2013; F1000Prime.com/4215956
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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.
DOI: 10.1111/j.1462-5822.2010.01431.x
PMID: 20070310
