Abstract
The central role of neutrophils in innate immunity and host defense has long been recognized, and the ability of these cells to efficiently engulf and kill invading bacteria has been extensively studied, as has the role of neutrophil apoptosis in resolution of the inflammatory response. In the past few years additional immunoregulatory properties of neutrophils were discovered, and it is now clear that these cells play a much greater role in control of the immune response than was previously appreciated. In this regard, it is noteworthy that Francisella tularensis is one of relatively few pathogens that can successfully parasitize neutrophils as well as macrophages, DC and epithelial cells. Herein we will review the mechanisms used by F. tularensis to evade elimination by neutrophils. We will also reprise effects of this pathogen on neutrophil migration and lifespan as compared with other infectious and inflammatory disease states. In addition, we will discuss the evidence which suggests that neutrophils contribute to disease progression rather than effective defense during tularemia, and consider whether manipulation of neutrophil migration or turnover may be suitable adjunctive therapeutic strategies.
Highlights
Inflammation Program and the Departments of Internal Medicine and Microbiology, University of Iowa and the VA Medical Center, Iowa City, IA, USA
In contrast to other leukocytes, neutrophils are short-lived and are preprogrammed to undergo constitutive apoptosis 18–24 h after release into circulation, and under normal circumstances, Polymorphonuclear leukocyte (PMN) apoptosis is further accelerated by phagocytosis and oxidant production (Watson et al, 1996; Kobayashi et al, 2003c; Kobayashi and Deleo, 2009)
PGE2 is produced by F. tularensis-infected macrophages and alveolar type II (ATII) cells (Woolard et al, 2007) and infected PMNs upregulate IL-1β (Schwartz et al, 2013), but the extent to which these agents contribute to PMN chemotaxis and phenotypic modulation during tularemia remains to be determined
Summary
Inflammation Program and the Departments of Internal Medicine and Microbiology, University of Iowa and the VA Medical Center, Iowa City, IA, USA. PGE2 is produced by F. tularensis-infected macrophages and ATII cells (Woolard et al, 2007) and infected PMNs upregulate IL-1β (Schwartz et al, 2013), but the extent to which these agents contribute to PMN chemotaxis and phenotypic modulation during tularemia remains to be determined.
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