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Multifaceted effects of F rancisella tularensis on human neutrophil function and lifespan
Author(s) -
Kinkead Lauren C.,
Allen LeeAnn H.
Publication year - 2016
Publication title -
immunological reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.839
H-Index - 223
eISSN - 1600-065X
pISSN - 0105-2896
DOI - 10.1111/imr.12445
Subject(s) - tularemia , francisella tularensis , biology , phagocytosis , antibody opsonization , microbiology and biotechnology , immunology , intracellular , pathogen , francisella , pathogenesis , chemotaxis , intracellular parasite , neutrophil extracellular traps , immune system , inflammation , virulence , opsonin , receptor , genetics , gene
Summary 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.