schliessen

Filtern

 

Bibliotheken

Killing activity of neutrophils is mediated through activation of proteases by K+ flux

According to the hitherto accepted view, neutrophils kill ingested microorganisms by subjecting them to high concentrations of highly toxic reactive oxygen species (ROS) and bringing about myeloperoxidase-catalysed halogenation. We show here that this simple scheme, which for many years has served a... Full description

Journal Title: Nature March 21, 2002, Vol.416(6878), p.291(7)
Main Author: Reeves, Emer P.
Other Authors: Lu, Hui , Jacobs, Hugues Lortat , Messina, Carlo G. M. , Bolsover, Steve , Gabella, Giorgio , Potma, Eric O. , Warley, Alice , Roes, Jurgen , Segal, Anthony W.
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 0028-0836
Zum Text:
SendSend as email Add to Book BagAdd to Book Bag
Staff View
recordid: gale_ofa187500434
title: Killing activity of neutrophils is mediated through activation of proteases by K+ flux
format: Article
creator:
  • Reeves, Emer P.
  • Lu, Hui
  • Jacobs, Hugues Lortat
  • Messina, Carlo G. M.
  • Bolsover, Steve
  • Gabella, Giorgio
  • Potma, Eric O.
  • Warley, Alice
  • Roes, Jurgen
  • Segal, Anthony W.
subjects:
  • Cathepsin G
  • Leukocyte Elastase
  • Granules
  • Vacuoles
  • Reactive Oxygen Species
  • Leukocytes (Neutrophilic)
  • Potassium
  • Other Cells (Leukocytes, Eosinophils, Basophils, Neutrophils, Platelets)
ispartof: Nature, March 21, 2002, Vol.416(6878), p.291(7)
description: According to the hitherto accepted view, neutrophils kill ingested microorganisms by subjecting them to high concentrations of highly toxic reactive oxygen species (ROS) and bringing about myeloperoxidase-catalysed halogenation. We show here that this simple scheme, which for many years has served as a satisfactory working hypothesis, is inadequate. We find that mice made deficient in neutrophil-granule proteases but normal in respect of superoxide production and iodinating capacity, are unable to resist staphylococcal and candidal infections. We also show that activation provokes the influx of an enormous concentration of ROS into the endocytic vacuole. The resulting accumulation of anionic charge is compensated for by a surge of K[sup.+] ions that cross the membrane in a pH-dependent manner. The consequent rise in ionic strength engenders the release of cationic granule proteins, including elastase and cathepsin G, from the anionic sulphated proteoglycan matrix. We show that it is the proteases, thus activated, that are primarily responsible for the destruction of the bacteria.
language: English
source:
identifier: ISSN: 0028-0836
fulltext: fulltext
issn:
  • 0028-0836
  • 00280836
url: Link


@attributes
ID1048435475
RANK0.06999999
NO1
SEARCH_ENGINEprimo_central_multiple_fe
SEARCH_ENGINE_TYPEPrimo Central Search Engine
LOCALfalse
PrimoNMBib
record
control
sourcerecordid187500434
sourceidgale_ofa
recordidTN_gale_ofa187500434
sourceformatXML
sourcesystemPC
pqid204512230
galeid187500434
display
typearticle
titleKilling activity of neutrophils is mediated through activation of proteases by K+ flux
creatorReeves, Emer P. ; Lu, Hui ; Jacobs, Hugues Lortat ; Messina, Carlo G. M. ; Bolsover, Steve ; Gabella, Giorgio ; Potma, Eric O. ; Warley, Alice ; Roes, Jurgen ; Segal, Anthony W.
ispartofNature, March 21, 2002, Vol.416(6878), p.291(7)
identifierISSN: 0028-0836
descriptionAccording to the hitherto accepted view, neutrophils kill ingested microorganisms by subjecting them to high concentrations of highly toxic reactive oxygen species (ROS) and bringing about myeloperoxidase-catalysed halogenation. We show here that this simple scheme, which for many years has served as a satisfactory working hypothesis, is inadequate. We find that mice made deficient in neutrophil-granule proteases but normal in respect of superoxide production and iodinating capacity, are unable to resist staphylococcal and candidal infections. We also show that activation provokes the influx of an enormous concentration of ROS into the endocytic vacuole. The resulting accumulation of anionic charge is compensated for by a surge of K[sup.+] ions that cross the membrane in a pH-dependent manner. The consequent rise in ionic strength engenders the release of cationic granule proteins, including elastase and cathepsin G, from the anionic sulphated proteoglycan matrix. We show that it is the proteases, thus activated, that are primarily responsible for the destruction of the bacteria.
languageEnglish
source
subjectCathepsin G ; Leukocyte Elastase ; Granules ; Vacuoles ; Reactive Oxygen Species ; Leukocytes (Neutrophilic) ; Potassium ; Other Cells (Leukocytes, Eosinophils, Basophils, Neutrophils, Platelets);
version11
lds50peer_reviewed
links
openurl$$Topenurl_article
openurlfulltext$$Topenurlfull_article
search
scope
0gale_onefileg
1gale_onefilea
2OneFile
creatorcontrib
0Reeves, Emer P
1Emer P. Reeves; Hui Lu; Hugues Lortat Jacobs; Carlo G. M. Messina; Steve Bolsover; Giorgio Gabella; Eric O. Potma; Alice Warley; Jurgen Roes; An ...
2Lu, Hui
3Jacobs, Hugues Lortat
4Messina, Carlo G. M
5Bolsover, Steve
6Gabella, Giorgio
7Potma, Eric O
8Warley, Alice
9Roes, Jurgen
10Segal, Anthony W
titleKilling activity of neutrophils is mediated through activation of proteases by K+ flux.
descriptionAccording to the hitherto accepted view, neutrophils kill ingested microorganisms by subjecting them to high concentrations of highly toxic reactive oxygen species (ROS) and bringing about myeloperoxidase-catalysed halogenation. We show here that this simple scheme, which for many years has served as a satisfactory working hypothesis, is inadequate. We find that mice made deficient in neutrophil-granule proteases but normal in respect of superoxide production and iodinating capacity, are unable to resist staphylococcal and candidal infections. We also show that activation provokes the influx of an enormous concentration of ROS into the endocytic vacuole. The resulting accumulation of anionic charge is compensated for by a surge of K[sup.+] ions that cross the membrane in a pH-dependent manner. The consequent rise in ionic strength engenders the release of cationic granule proteins, including elastase and cathepsin G, from the anionic sulphated proteoglycan matrix. We show that it is the proteases, thus activated, that are primarily responsible for the destruction of the bacteria.
general
0English
1Nature Publishing Group
2Cengage Learning, Inc.
sourceidgale_ofa
recordidgale_ofa187500434
issn
00028-0836
100280836
rsrctypearticle
creationdate2002
recordtypearticle
addtitleNature
searchscopeOneFile
lsr30VSR-Enriched:[galeid, pqid, eissn, pages, subject, doi]
sort
titleKilling activity of neutrophils is mediated through activation of proteases by K+ flux.
authorReeves, Emer P. ; Lu, Hui ; Jacobs, Hugues Lortat ; Messina, Carlo G. M. ; Bolsover, Steve ; Gabella, Giorgio ; Potma, Eric O. ; Warley, Alice ; Roes, Jurgen ; Segal, Anthony W.
creationdate20020321
facets
frbrgroupid8507958607217645908
frbrtype5
languageeng
creationdate2002
collectionOneFile (GALE)
prefilterarticles
rsrctypearticles
creatorcontrib
0Reeves, Emer P.
1Lu, Hui
2Jacobs, Hugues Lortat
3Messina, Carlo G. M.
4Bolsover, Steve
5Gabella, Giorgio
6Potma, Eric O.
7Warley, Alice
8Roes, Jurgen
9Segal, Anthony W.
jtitleNature
toplevelpeer_reviewed
frbr
t2
k12002
k200280836
k4416
k56878
k6291
k7nature
k8killing activity of neutrophils is mediated through activation of proteases by k flux
k9killingactivityofneukflux
k12killingactivityofneutroph
k15emerpreeves
k16reevesemerp
delivery
delcategoryRemote Search Resource
fulltextfulltext
ranking
booster11
booster21
pcg_typeaggregator
addata
au
0Reeves, Emer P.
1Lu, Hui
2Jacobs, Hugues Lortat
3Messina, Carlo G. M.
4Bolsover, Steve
5Gabella, Giorgio
6Potma, Eric O.
7Warley, Alice
8Roes, Jurgen
9Segal, Anthony W.
atitleKilling activity of neutrophils is mediated through activation of proteases by K+ flux.
jtitleNature
risdate20020321
volume416
issue6878
spage291
issn0028-0836
genrearticle
ristypeJOUR
abstractAccording to the hitherto accepted view, neutrophils kill ingested microorganisms by subjecting them to high concentrations of highly toxic reactive oxygen species (ROS) and bringing about myeloperoxidase-catalysed halogenation. We show here that this simple scheme, which for many years has served as a satisfactory working hypothesis, is inadequate. We find that mice made deficient in neutrophil-granule proteases but normal in respect of superoxide production and iodinating capacity, are unable to resist staphylococcal and candidal infections. We also show that activation provokes the influx of an enormous concentration of ROS into the endocytic vacuole. The resulting accumulation of anionic charge is compensated for by a surge of K[sup.+] ions that cross the membrane in a pH-dependent manner. The consequent rise in ionic strength engenders the release of cationic granule proteins, including elastase and cathepsin G, from the anionic sulphated proteoglycan matrix. We show that it is the proteases, thus activated, that are primarily responsible for the destruction of the bacteria.
pubNature Publishing Group
lad01gale_ofa
pages291-297
doi10.1038/416291a
eissn14764687
date2002-03-21