Chlamydia pneumoniae Multiply in Neutrophil Granulocytes and Delay Their Spontaneous Apoptosis1
@article{vanZandbergen2004ChlamydiaPM,
title={Chlamydia pneumoniae Multiply in Neutrophil Granulocytes and Delay Their Spontaneous Apoptosis1},
author={Ger van Zandbergen and Jens Gieffers and Henning Kothe and Jan Rupp and Anna‐Lena Bollinger and Eresso Aga and Matthias Klinger and Helmut Brade and Klaus Dalhoff and Matthias Maass and Werner Solbach and Tam{\'a}s Laskay},
journal={The Journal of Immunology},
year={2004},
volume={172},
pages={1768 - 1776},
url={https://api.semanticscholar.org/CorpusID:27422510}
}Data show that, in contrast to other microbial pathogens that drive phagocytes into apoptosis to escape killing, Cp can extend the life span of neutrophil granulocytes, making them suitable host cells for survival and multiplication within the first hours/days after infection.
171 Citations
Chlamydia pneumoniae Hides inside Apoptotic Neutrophils to Silently Infect and Propagate in Macrophages
- 2009
Biology, Medicine
The data suggest that C. pneumoniae uses neutrophil granulocytes to be silently taken up by long-lived macrophages, which allows for efficient propagation and immune protection within the human host.
Mechanisms of apoptosis inhibition in Chlamydia pneumoniae-infected neutrophils.
- 2015
Biology, Medicine
Anaplasma phagocytophilum Delay of Neutrophil Apoptosis through the p38 Mitogen-Activated Protein Kinase Signal Pathway
- 2005
Biology, Medicine
It is demonstrated that antiapoptotic Mcl-1 protein (Bcl-2 family) expression is maintained and that inhibition of procaspase-3 processing occurs in A. phagocytophilum-infected human neutrophils, and an important role for active infection is demonstrated by the additional delay in apoptosis with intracellular growth and the refractory abrogation of this response by the p38 MAPK inhibitor 3 to 6 h after neutrophil
Polymorphonuclear Neutrophils Improve Replication of Chlamydia pneumoniae In Vivo upon MyD88-Dependent Attraction1
- 2005
Biology, Medicine
It is found that PMN are infected and enhance the replication of C. pneumoniae in epithelial cells, and the lower chlamydial burden in MyD88-deficient mice can be explained by the failure to recruit PMN, which can be reproduced in wild-type mice by depletion of GR1+ cells.
echanisms of apoptosis inhibition in Chlamydia neumoniae-infected neutrophils
- 2015
Biology, Medicine
It is presented evidence that activation of the PI3K/Akt and ERK1/2 pathways are essential to initiate the apoptosis delay in C. pneumoniae-infected neutrophils.
Chlamydia pneumoniae Inhibits Activated Human T Lymphocyte Proliferation by the Induction of Apoptotic and Pyroptotic Pathways
- 2011
Biology, Medicine
Findings are consistent with the conclusion that C. pneumoniae could induce a local T cell immunosuppression and inflammatory response revealing a possible host–pathogen scenario that would support both persistence and inflammation.
Brucella abortus Induces the Premature Death of Human Neutrophils through the Action of Its Lipopolysaccharide
- 2015
Biology, Medicine
A mechanism for neutropenia in chronic brucellosis is suggested and a novel Brucella-host cross-talk through which B. abortus is able to hinder the innate function of PMN is revealed.
Neutrophil granulocytes as host cells and transport vehicles for intracellular pathogens: apoptosis as infection-promoting factor.
- 2008
Biology, Medicine
PathwaysInduction of Apoptotic and Pyroptotic Human T Lymphocyte Proliferation by the Inhibits Activated Chlamydia pneumoniae
- 2011
Medicine, Biology
It was found that C. pneumoniae organisms inhibited activated but not nonactivated human T cell proliferation, indicating that both apoptotic and pyroptotic cellular death pathways were activated after pathogen–T cell interactions, consistent with the conclusion that C pneumoniae could induce a local T cell immunosuppression and in-ammatory response.
Neisseria gonorrhoeae-Mediated Inhibition of Apoptotic Signalling in Polymorphonuclear Leukocytes
- 2011
Biology, Medicine
An HL-60 myeloid leukemia cell culture model for PMN infection is developed and validated and it is shown that N. gonorrhoeae infection alone does not induce apoptosis, but actively inhibits apoptosis induced by multiple stimuli to prolong PMN survival and potentially facilitate bacterial survival, replication, and transmission.
55 References
Inhibition of the Spontaneous Apoptosis of Neutrophil Granulocytes by the Intracellular Parasite Leishmania major1
- 2002
Biology, Medicine
In vitro coincubation experiments indicate that Leishmania induce an increased survival of neutrophil granulocytes both in vitro and in vivo, and strongly suggests that infection with LeishMania prolongs the survival time of neutrophic neutrophils also in vivo.
Characterization of Antiapoptotic Activities ofChlamydia pneumoniae in Human Cells
- 2001
Biology, Medicine
The results show that C. pneumoniae is capable of interfering with the host cell's apoptotic apparatus at probably at least two steps in signal transduction and might explain the propensity of these bacteria to cause chronic infections in humans.
Neutrophils undergo apoptosis following ingestion of Escherichia coli.
- 1996
Biology, Medicine
It is demonstrated for the first time that E. coli induces PMN apoptosis through an oxygen-dependent mechanism and the removal of effete PMN by the process of apoptosis rather than necrosis may be teleologically beneficial during Gram-negative septicemia.
Phagocytosis of Candida albicans induces apoptosis of human neutrophils.
- 2000
Biology, Medicine
An important physiologic role for host-pathogen interactions in the resolution of inflammation is demonstrated and the response to an invading pathogen is suggested to be an important stimulus to the restoration of normal immunologic homeostasis.
Interaction between Chlamydia spp. and human polymorphonuclear leukocytes in vitro
- 1986
Biology, Medicine
The ability of a small percentage of infecting chlamydiae to maintain infectivity in PMN for at least several hours may enable these organisms subsequently to establish productive infection in permissive host cells.
Intracellular Survival of Leishmania major in Neutrophil Granulocytes after Uptake in the Absence of Heat-Labile Serum Factors
- 2002
Biology, Medicine
The finding that intact parasites were seen in PMN isolated from the skin of infected mice, suggest that PMN can serve as host cells for the intracellular survival of Leishmania within the first hours or days after infection.
Chlamydia pneumoniae Infects and Multiplies in Lymphocytes In Vitro
- 2001
Biology, Medicine
Findings reveal a new infection site for C. pneumoniae, i.e., lymphocytes, and indicate that T cells could be one of the host cells for this bacterial infection.
Inhibition of Apoptosis in Chlamydia-infected Cells: Blockade of Mitochondrial Cytochrome c Release and Caspase Activation
- 1998
Biology, Medicine
A chlamydial antiapoptosis mechanism(s) is identified that will help define chlamYDial pathogenesis and may also provide information about the central mechanisms regulating host cell apoptosis.
Leishmania Promastigotes Release a Granulocyte Chemotactic Factor and Induce Interleukin-8 Release but Inhibit Gamma Interferon-Inducible Protein 10 Production by Neutrophil Granulocytes
- 2002
Biology, Medicine
Infection with Leishmania promastigotes leads to PMN accumulation via the production of a chemotactic factor by the parasites, and this effect is amplified by the induction of IL-8 production in PMN, and the inhibition of IP-10 production can lead to prevention of NK cell activation.
Infection of Human Endothelial Cells with Chlamydia pneumoniae Stimulates Transendothelial Migration of Neutrophils and Monocytes
- 1999
Medicine, Biology
Results from this study indicate that the passage history of C. pneumoniae may play a role in the divergence of stimulatory activities observed among isolates in human endothelial cells, and suggest that the upregulation of IL-8 and MCP-1 in endothelium cells may be unique to C. tuberculosis.








