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Immunol Rev. 2016 Sep;273(1):266-81. doi: 10.1111/imr.12445.

Multifaceted effects of Francisella tularensis on human neutrophil function and lifespan.

Kinkead LC1,2, Allen LA1,2,3,4.

Author information

1
Inflammation Program, University of Iowa, Coralville, IA, USA.
2
Department of Microbiology, University of Iowa, Coralville, IA, USA.
3
Department of Internal Medicine, University of Iowa, Coralville, IA, USA.
4
VA Medical Center, Iowa City, IA, USA.

Abstract

Francisella tularensis in an intracellular bacterial pathogen that causes a potentially lethal disease called tularemia. Studies performed nearly 100 years ago revealed that neutrophil accumulation in infected tissues correlates directly with the extent of necrotic damage during F. tularensis infection. However, the dynamics and details of bacteria-neutrophil interactions have only recently been studied in detail. Herein, we review current understanding regarding the mechanisms that recruit neutrophils to F. tularensis-infected lungs, opsonization and phagocytosis, evasion and inhibition of neutrophil defense mechanisms, as well as the ability of F. tularensis to prolong neutrophil lifespan. In addition, we discuss distinctive features of the bacterium, including its ability to act at a distance to alter overall neutrophil responsiveness to exogenous stimuli, and the evidence which suggests that macrophages and neutrophils play distinct roles in tularemia pathogenesis, such that macrophages are major vehicles for intracellular growth and dissemination, whereas neutrophils drive tissue destruction by dysregulation of the inflammatory response.

KEYWORDS:

NADPH oxidase; apoptosis; inflammation; neutrophils; phagocytosis; tularemia

PMID:
27558340
PMCID:
PMC5000853
DOI:
10.1111/imr.12445
[Indexed for MEDLINE]
Free PMC Article

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