Alteration of Polymorphonuclear Neutrophil Surface Receptor Expression and Migratory Activity After Isolation: Comparison of Whole Blood and Isolated PMN Preparations from Normal and Postfracture Trauma Patients

Pallister, Ian; Bhatia, R.; Katpalli, Gopi; Allison, Dawn; Parker, Clare; Topley, Nicholas

doi:10.1097/01.ta.0000215583.08765.ce

Cited by 21 publications

(16 citation statements)

References 29 publications

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“…During the first days after trauma, circulating PMNs prove to be primed, resulting in not only an increased migratory capacity but also in enhanced cytotoxic functions [33,[40][41][42]. The levels of neutrophil elastase as indicator of systemic activation of PMNs rise shortly after injury [15].…”

Section: Cellular Responsementioning

confidence: 98%

Postinjury immune monitoring: can multiple organ failure be predicted?

Visser¹,

Pillay²,

Koenderman³

et al. 2008

Current Opinion in Critical Care

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Section: Cellular Responsementioning

confidence: 98%

Postinjury immune monitoring: can multiple organ failure be predicted?

Visser¹,

Pillay²,

Koenderman³

et al. 2008

Current Opinion in Critical Care

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“…In contrast, Thorén et al (26) recently reported that NK cells accelerate spontaneous apoptosis of isolated PMNs. In this study, to avoid the PMN isolation procedures that have been reported to alter PMN responses (21,42,43), we analyzed PMN apoptosis by flow cytometry in whole-blood conditions. In these conditions, with whole-blood PMN activation by GG, a polysaccharide extracted from A. fumigatus, we demonstrated that NK cells are a critical trigger of PMN apoptosis.…”

Section: Discussionmentioning

confidence: 99%

A Polysaccharide Virulence Factor of a Human Fungal Pathogen Induces Neutrophil Apoptosis via NK Cells

Robinet

Baychelier

Fontaine

et al. 2014

The Journal of Immunology

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Aspergillus fumigatus is an opportunistic human fungal pathogen that sheds galactosaminogalactan (GG) into the environment. Polymorphonuclear neutrophils (PMNs) and NK cells are both part of the first line of defense against pathogens. We recently reported that GG induces PMN apoptosis. In this study, we show that PMN apoptosis occurs via a new NK cell–dependent mechanism. Reactive oxygen species, induced by the presence of GG, play an indispensable role in this apoptotic effect by increasing MHC class I chain–related molecule A expression at the PMN surface. This increased expression enables interaction between MHC class I chain–related molecule A and NKG2D, leading to NK cell activation, which in turn generates a Fas-dependent apoptosis-promoting signal in PMNs. Taken together, our results demonstrate that the crosstalk between PMNs and NK cells is essential to GG-induced PMN apoptosis. NK cells might thus play a role in the induction of PMN apoptosis in situations such as unexplained neutropenia or autoimmune diseases.

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“…4,5 The relationship between priming that has occurred, residual priming potential, and functional activity are areas which currently remain ill-defined. 23 Thus, these primed PMN are capable of causing increased tissue damage by degranulation and respiratory burst activity once they have homed to the lung and site of injury in large numbers and are activated by local factors. Targeting PMN degranulation and preventing the sequestration of large numbers of primed/activated PMN in the lung and other tissues may provide potential therapeutic avenues in preventing the development of ARDS/MOF.…”

Section: Discussionmentioning

confidence: 99%