Multiple mechanisms of NADPH oxidase inhibition by type A and type B Francisella tularensis

@article{McCaffrey2010MultipleMO,
  title={Multiple mechanisms of NADPH oxidase inhibition by type A and type B Francisella tularensis},
  author={Ramona L. McCaffrey and Justin T. Schwartz and Stephen R. Lindemann and Jessica G. Moreland and Blake W. Buchan and Bradley D. Jones and Lee-Ann H Allen},
  journal={Journal of Leukocyte Biology},
  year={2010},
  volume={88}
}
Ft is a facultative intracellular pathogen that infects many cell types, including neutrophils. In previous work, we demonstrated that the type B Ft strain LVS disrupts NADPH oxidase activity throughout human neutrophils, but how this is achieved is incompletely defined. Here, we used several type A and type B strains to demonstrate that Ft‐mediated NADPH oxidase inhibition is more complex than appreciated previously. We confirm that phagosomes containing Ft opsonized with AS exclude… 
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References

SHOWING 1-10 OF 85 REFERENCES

Inhibition of the human neutrophil NADPH oxidase by Coxiella burnetii.

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 LVS evades killing by human neutrophils via inhibition of the respiratory burst and phagosome escape

The data are the first demonstration of a facultative intracellular pathogen, which disrupts the oxidative burst and escapes the phagosome to evade elimination inside neutrophils, and as such, define a novel mechanism of virulence.

Leishmania donovani  lipophosphoglycan blocks NADPH oxidase assembly at the phagosome membrane

By remodelling their intracellular habitat, L.’donovani promastigotes prevent the assembly of a functional phagosomal NADPH oxidase complex, thereby evading an important host innate defence mechanism.

Acid Phosphatases Do Not Contribute to the Pathogenesis of Type A Francisella tularensis

The acid phosphatases AcpA, AcpB, and AcpC do not contribute to intracellular pathogenesis and do not play a major role in the virulence of type A Francisella strains.

Characterization and Sequencing of a Respiratory Burst-inhibiting Acid Phosphatase from Francisella tularensis(*)

This is the first report describing the cloning and sequencing of a burst-inhibiting acid phosphatase from the facultative intracellular bacterium, Francisella tularensis, and the complete nucleotide sequence of the gene acpA, encoding AcpA and the deduced primary structure of its encoded polypeptide is reported.

Mechanisms of evasion of neutrophil killing by Anaplasma phagocytophilum

A. phagocytophilum extends the life of its otherwise short-lived host cell by dysregulating neutrophil gene expression and molecular machinery to potentially maximize its survival and dissemination within its mammalian host.

Identification of LpxL, a Late Acyltransferase of Francisella tularensis

ABSTRACT Lipopolysaccharide (LPS) is a major component of the outer membrane of gram-negative bacteria, and the lipid A region of LPS mediates stimulation of the immune system in a…

Regulation and termination of NADPH oxidase activity

This review considers mechanisms that have been proposed to terminate the phagocyte respiratory burst oxidase in human neutrophils and finds changes in the phosphorylation state of p47phox and in the species of nucleotide bound to Rac seem to be the dominant factors in deactivation.

Assembly of the phagocyte NADPH oxidase: molecular interaction of oxidase proteins

The key features of each NADPH oxidase protein are described and the current understanding of the specific molecular interactions occurring between these proteins are summarized, focusing on the role these protein:protein binding interactions play in the NADPH oxidation assembly process.
...