To activate or not to activate: distinct strategies used by Helicobacter pylori and Francisella tularensis to modulate the NADPH oxidase and survive in human neutrophils

@article{Allen2007ToAO,
  title={To activate or not to activate: distinct strategies used by Helicobacter pylori and Francisella tularensis to modulate the NADPH oxidase and survive in human neutrophils},
  author={Lee-Ann H Allen and Ramona L. McCaffrey},
  journal={Immunological Reviews},
  year={2007},
  volume={219}
}
Summary:  Neutrophils accumulate rapidly at sites of infection, and the ability of these cells to phagocytose and kill microorganisms is an essential component of the innate immune response. Relatively few microbial pathogens are able to evade neutrophil killing. Herein, we describe the novel strategies used by Helicobacter pylori and Francisella tularensis to disrupt neutrophil function, with a focus on assembly and activation of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. 
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66 Citations
Highly Influential Citations
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66 Citations

Francisella tularensis Genes Required for Inhibition of the Neutrophil Respiratory Burst and Intramacrophage Growth Identified by Random Transposon Mutagenesis of Strain LVS

It is shown that uracil auxotrophy has cell type-specific effects on the fate of Francisella bacteria, and random transposon mutagenesis is used to identify LVS genes that affect neutrophil activation.

Francisella tularensis intracellular survival: to eat or to die.

Cell intrinsic functions of neutrophils and their manipulation by pathogens.

Multifaceted effects of Francisella tularensis on human neutrophil function and lifespan

  • Lauren C. KinkeadL. Allen
  • Biology, Medicine
    Immunological reviews
  • 2016
Current understanding regarding the mechanisms that recruit neutrophils to F. tularensis and distinctive features of the bacterium are reviewed, including its ability to act at a distance to alter overall neutrophil responsiveness to exogenous stimuli, and the evidence which suggests that macrophages and neutrophIL play distinct roles in tularemia pathogenesis.

Loops and networks in control of Francisella tularensis virulence.

The unraveling secrets of the regulatory cascades governing the regulation of virulence of F. tularensis will be discussed along with future challenges yet to be solved.

Antioxidant Defenses of Francisella tularensis Modulate Macrophage Function and Production of Proinflammatory Cytokines*

Novel pathogenic mechanisms adopted by F. tularensis to modulate macrophage innate immune functions to create an environment permissive for its intracellular survival and growth are revealed.

Role of neutrophils and NADPH phagocyte oxidase in host defense against respiratory infection with virulent Francisella tularensis in mice.

The interaction of Francisella tularensis with lung epithelial cells

Following intranasal inoculation of C57BL/6 mice, Francisella localized to the alveolus and replicated within alveolar type II epithelial cells.

EmrA1 membrane fusion protein of Francisella tularensis LVS is required for resistance to oxidative stress, intramacrophage survival and virulence in mice

The results demonstrate that the emrA1 mutant is highly sensitive to oxidants and several antimicrobial agents, and exhibits diminished intramacrophage growth that can be restored to wild‐type F. tularensis levels by either transcomplementation, inhibition of ROS generation or infection in NADPH oxidase deficient macrophages.

Extracellular adenosine enhances the ability of PMNs to kill Streptococcus pneumoniae by inhibiting IL-10 production

It is demonstrated that CD73 regulates PMN anti-microbial phenotype during pneumococcal pneumonia by promoting the ability of PMNs to kill Streptococcus pneumoniae by blunting IL-10 production.
...

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