Proteomic and oxPTM analysis of neutrophil extracellular traps

Y. Li, H.J. Wright, A.R. Pitt, I.L.C. Chapple, C.M. Spickett

Research output: Contribution to journalMeeting abstract

Abstract

As the most abundant type of white blood cells in mammals, neutrophils form an essential part of the innate immune system. They employ three strategies to eliminate invading microbes: phagocytosis of engulfing bacteria, degranulation involving release of soluble anti-microbial compounds, and a recently discovered mechanism called neutrophil extracellular traps (NETs). NET formation seems to be the consequence of a novel form of active cell death that is neither necrosis nor apoptosis, and they form as part of an innate immune response at sites of acute inflammation. Early work suggested that this cell death program depends on the generation of reactive oxygen species by NADPH oxidase, suggesting the role of a redox-regulated cell signalling pathway. A more recent study has demonstrated the requirement specifically for HOCl production. To investigate further the molecular makeup of NETs and the role of HOCl and signalling mechanisms, we have utilized tandem mass spectrometry techniques to determine the proteins present in NETs and to map the occurrence of oxidative modifications to these proteins. We observed a number of the proteins that have previously been reported as associated with NETs (for example myeloperoxidase, catalase and actin), plus more than one hundred of new proteins that may be associated with NETs including moesin, neuroleukin, annexin and serpin B4. These findings provide a more detailed molecular composition of NETs and a deeper understanding of the role of HOCl-based oxidation in the mechanisms triggering NET release.
LanguageEnglish
Article number0583
PagesS170
Number of pages1
JournalFree Radical Biology and Medicine
Volume53
Issue numberSupplement 1
DOIs
Publication statusPublished - Sep 2012
EventSociety for Free Radical Research International 16th Biennial Meeting - Imperial College London, London, United Kingdom
Duration: 6 Sep 20129 Sep 2012

Fingerprint

Proteomics
Cell death
Proteins
Cell signaling
Serpins
Glucose-6-Phosphate Isomerase
Annexins
Mammals
NADPH Oxidase
Immune system
Catalase
Peroxidase
Mass spectrometry
Actins
Reactive Oxygen Species
Bacteria
Blood
Cell Death
Cells
Apoptosis

Cite this

Li, Y. ; Wright, H.J. ; Pitt, A.R. ; Chapple, I.L.C. ; Spickett, C.M. / Proteomic and oxPTM analysis of neutrophil extracellular traps. In: Free Radical Biology and Medicine. 2012 ; Vol. 53, No. Supplement 1. pp. S170.
@article{97effa7b4ff94ef98cd52c931f8d6ed5,
title = "Proteomic and oxPTM analysis of neutrophil extracellular traps",
abstract = "As the most abundant type of white blood cells in mammals, neutrophils form an essential part of the innate immune system. They employ three strategies to eliminate invading microbes: phagocytosis of engulfing bacteria, degranulation involving release of soluble anti-microbial compounds, and a recently discovered mechanism called neutrophil extracellular traps (NETs). NET formation seems to be the consequence of a novel form of active cell death that is neither necrosis nor apoptosis, and they form as part of an innate immune response at sites of acute inflammation. Early work suggested that this cell death program depends on the generation of reactive oxygen species by NADPH oxidase, suggesting the role of a redox-regulated cell signalling pathway. A more recent study has demonstrated the requirement specifically for HOCl production. To investigate further the molecular makeup of NETs and the role of HOCl and signalling mechanisms, we have utilized tandem mass spectrometry techniques to determine the proteins present in NETs and to map the occurrence of oxidative modifications to these proteins. We observed a number of the proteins that have previously been reported as associated with NETs (for example myeloperoxidase, catalase and actin), plus more than one hundred of new proteins that may be associated with NETs including moesin, neuroleukin, annexin and serpin B4. These findings provide a more detailed molecular composition of NETs and a deeper understanding of the role of HOCl-based oxidation in the mechanisms triggering NET release.",
author = "Y. Li and H.J. Wright and A.R. Pitt and I.L.C. Chapple and C.M. Spickett",
year = "2012",
month = "9",
doi = "10.1016/j.freeradbiomed.2012.08.356",
language = "English",
volume = "53",
pages = "S170",
journal = "Free Radical Biology and Medicine",
issn = "0891-5849",
publisher = "Elsevier",
number = "Supplement 1",

}

Proteomic and oxPTM analysis of neutrophil extracellular traps. / Li, Y.; Wright, H.J.; Pitt, A.R.; Chapple, I.L.C.; Spickett, C.M.

In: Free Radical Biology and Medicine, Vol. 53, No. Supplement 1, 0583, 09.2012, p. S170.

Research output: Contribution to journalMeeting abstract

TY - JOUR

T1 - Proteomic and oxPTM analysis of neutrophil extracellular traps

AU - Li, Y.

AU - Wright, H.J.

AU - Pitt, A.R.

AU - Chapple, I.L.C.

AU - Spickett, C.M.

PY - 2012/9

Y1 - 2012/9

N2 - As the most abundant type of white blood cells in mammals, neutrophils form an essential part of the innate immune system. They employ three strategies to eliminate invading microbes: phagocytosis of engulfing bacteria, degranulation involving release of soluble anti-microbial compounds, and a recently discovered mechanism called neutrophil extracellular traps (NETs). NET formation seems to be the consequence of a novel form of active cell death that is neither necrosis nor apoptosis, and they form as part of an innate immune response at sites of acute inflammation. Early work suggested that this cell death program depends on the generation of reactive oxygen species by NADPH oxidase, suggesting the role of a redox-regulated cell signalling pathway. A more recent study has demonstrated the requirement specifically for HOCl production. To investigate further the molecular makeup of NETs and the role of HOCl and signalling mechanisms, we have utilized tandem mass spectrometry techniques to determine the proteins present in NETs and to map the occurrence of oxidative modifications to these proteins. We observed a number of the proteins that have previously been reported as associated with NETs (for example myeloperoxidase, catalase and actin), plus more than one hundred of new proteins that may be associated with NETs including moesin, neuroleukin, annexin and serpin B4. These findings provide a more detailed molecular composition of NETs and a deeper understanding of the role of HOCl-based oxidation in the mechanisms triggering NET release.

AB - As the most abundant type of white blood cells in mammals, neutrophils form an essential part of the innate immune system. They employ three strategies to eliminate invading microbes: phagocytosis of engulfing bacteria, degranulation involving release of soluble anti-microbial compounds, and a recently discovered mechanism called neutrophil extracellular traps (NETs). NET formation seems to be the consequence of a novel form of active cell death that is neither necrosis nor apoptosis, and they form as part of an innate immune response at sites of acute inflammation. Early work suggested that this cell death program depends on the generation of reactive oxygen species by NADPH oxidase, suggesting the role of a redox-regulated cell signalling pathway. A more recent study has demonstrated the requirement specifically for HOCl production. To investigate further the molecular makeup of NETs and the role of HOCl and signalling mechanisms, we have utilized tandem mass spectrometry techniques to determine the proteins present in NETs and to map the occurrence of oxidative modifications to these proteins. We observed a number of the proteins that have previously been reported as associated with NETs (for example myeloperoxidase, catalase and actin), plus more than one hundred of new proteins that may be associated with NETs including moesin, neuroleukin, annexin and serpin B4. These findings provide a more detailed molecular composition of NETs and a deeper understanding of the role of HOCl-based oxidation in the mechanisms triggering NET release.

U2 - 10.1016/j.freeradbiomed.2012.08.356

DO - 10.1016/j.freeradbiomed.2012.08.356

M3 - Meeting abstract

VL - 53

SP - S170

JO - Free Radical Biology and Medicine

T2 - Free Radical Biology and Medicine

JF - Free Radical Biology and Medicine

SN - 0891-5849

IS - Supplement 1

M1 - 0583

ER -