Molecular definition of distinct cytoskeletal structures involved in complement- and Fc receptor-mediated phagocytosis in macrophages
How cytoskeletal proteins associate with phagosomes containing complement-opsonized zymosan (COZ) particles or IgG beads in phorbol-myristateacetate-treated peritoneal macrophages is examined.
Francisella tularensis LVS evades killing by human neutrophils via inhibition of the respiratory burst and phagosome escape
- R. McCaffrey, L. Allen
- Biology, MedicineJournal of Leukocyte Biology
- 1 December 2006
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.
Identification of migR, a Regulatory Element of the Francisella tularensis Live Vaccine Strain iglABCD Virulence Operon Required for Normal Replication and Trafficking in Macrophages
- B. Buchan, R. McCaffrey, S. Lindemann, L. Allen, B. Jones
- BiologyInfection and Immunity
- 6 April 2009
MigR, a gene that regulates expression of the iglABCD operon and is essential for bacterial growth in MDMs and also contributes to the blockade of neutrophil NADPH oxidase activity is identified.
Virulent Strains of Helicobacter pylori Demonstrate Delayed Phagocytosis and Stimulate Homotypic Phagosome Fusion in Macrophages
- L. Allen, L. Schlesinger, B. Kang
- BiologyJournal of Experimental Medicine
- 3 January 2000
The data suggest that megasome formation is an important feature of H. pylori pathogenesis and uses an unusual mechanism to avoid phagocytic killing: delayed entry followed by homotypic phagosome fusion.
Francisella tularensis: taxonomy, genetics, and Immunopathogenesis of a potential agent of biowarfare.
- Molly K. McLendon, M. Apicella, L. Allen
- Biology, MedicineAnnual Review of Microbiology
- 11 September 2006
This review summarizes what is known about the pathogenesis of tularemia with a focus on bacterial surface components such as lipopolysaccharide and capsule as well as information obtained from the F. tularensis SCHU S4 genome.
Regulation of Human Neutrophil Apoptosis and Lifespan in Health and Disease
- J. McCracken, L. Allen
- Biology, MedicineJournal of Cell Death
- 8 May 2014
Recent advances in the understanding of the molecular mechanisms of neutrophil apoptosis are reprise with a focus on regulatory factors and pathway intermediates that are specific to this cell type.
Francisella tularensis Schu S4 O-Antigen and Capsule Biosynthesis Gene Mutants Induce Early Cell Death in Human Macrophages
- S. Lindemann, Kaitian Peng, B. Jones
- BiologyInfection and Immunity
- 15 November 2010
Microscopic and quantitative analyses of macrophages infected with mutant bacteria revealed that these macrophage exhibited signs of cell death much earlier than those infected with Schu S4, suggesting that FTT1236, F TT1237, and FTT 1238 are important for polysaccharide biosynthesis and that the Francisella O antigen, capsule, or both are importantfor avoiding the early induction of macphage death and the destruction of the replicative niche.
Multiple mechanisms of NADPH oxidase inhibition by type A and type B Francisella tularensis
- R. McCaffrey, Justin T. Schwartz, L. Allen
- BiologyJournal of Leukocyte Biology
- 1 October 2010
Several type A and type B Ft strains are used to demonstrate that Ft‐mediated NADPH oxidase inhibition is more complex than appreciated previously, and data strongly suggest that this is a central aspect of virulence.
Helicobacter pylori Disrupts NADPH Oxidase Targeting in Human Neutrophils to Induce Extracellular Superoxide Release1
- L. Allen, Benjamin R. Beecher, J. T. Lynch, Olga V. Rohner, Lara M. Wittine
- BiologyJournal of Immunology
- 15 March 2005
It is concluded that disruption of NADPH oxidase targeting allows unopsonized Hp to escape phagocytic killing, and the hypothesis that bacteria and PMNs act in concert to damage the gastric mucosa is supported.
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