Neutrophils and redox stress in the pathogenesis of autoimmune disease
Allbwn ymchwil: Cyfraniad at gyfnodolyn › Erthygl adolygu › adolygiad gan gymheiriaid
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Yn: Free radical biology & medicine, Cyfrol 125, 09.2018, t. 25-35.
Allbwn ymchwil: Cyfraniad at gyfnodolyn › Erthygl adolygu › adolygiad gan gymheiriaid
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T1 - Neutrophils and redox stress in the pathogenesis of autoimmune disease
AU - Glennon-Alty, Laurence
AU - Hackett, Angela P
AU - Chapman, Elinor A
AU - Wright, Helen L
N1 - Copyright © 2018 Elsevier Inc. All rights reserved.
PY - 2018/9
Y1 - 2018/9
N2 - Polymorphonuclear leukocytes, or neutrophils, are specialist phagocytic cells of the innate immune system. Their primary role is host defence against micro-organisms, which they kill via phagocytosis, followed by release of reactive oxygen species (ROS) and proteolytic enzymes within the phagosome. ROS are generated via the action of the NADPH oxidase (also known as NOX2), in a process termed the 'Respiratory Burst'. This process consumes large amounts of oxygen, which is converted into the highly-reactive superoxide radical O2- and H2O2. Subsequent activation of myeloperoxidase (MPO) generates secondary oxidants and chloroamines that are highly microbiocidal in nature, which together with proteases such as elastase and gelatinase provide a toxic intra-phagosomal environment able to kill a broad range of micro-organisms. However, under certain circumstances such as during an auto-immune response, neutrophils can be triggered to release ROS and proteases extracellularly causing damage to host tissues, modification of host proteins, lipids and DNA and dysregulation of oxidative homeostasis. This review describes the range of ROS species produced by human neutrophils with a focus on the implications of neutrophil redox products in autoimmune inflammation.
AB - Polymorphonuclear leukocytes, or neutrophils, are specialist phagocytic cells of the innate immune system. Their primary role is host defence against micro-organisms, which they kill via phagocytosis, followed by release of reactive oxygen species (ROS) and proteolytic enzymes within the phagosome. ROS are generated via the action of the NADPH oxidase (also known as NOX2), in a process termed the 'Respiratory Burst'. This process consumes large amounts of oxygen, which is converted into the highly-reactive superoxide radical O2- and H2O2. Subsequent activation of myeloperoxidase (MPO) generates secondary oxidants and chloroamines that are highly microbiocidal in nature, which together with proteases such as elastase and gelatinase provide a toxic intra-phagosomal environment able to kill a broad range of micro-organisms. However, under certain circumstances such as during an auto-immune response, neutrophils can be triggered to release ROS and proteases extracellularly causing damage to host tissues, modification of host proteins, lipids and DNA and dysregulation of oxidative homeostasis. This review describes the range of ROS species produced by human neutrophils with a focus on the implications of neutrophil redox products in autoimmune inflammation.
KW - Animals
KW - Autoimmune Diseases/etiology
KW - Humans
KW - Neutrophils/pathology
KW - Oxidation-Reduction
KW - Oxidative Stress
KW - Reactive Oxygen Species/metabolism
U2 - 10.1016/j.freeradbiomed.2018.03.049
DO - 10.1016/j.freeradbiomed.2018.03.049
M3 - Review article
C2 - 29605448
VL - 125
SP - 25
EP - 35
JO - Free radical biology & medicine
JF - Free radical biology & medicine
SN - 0891-5849
ER -