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ATP release from dying autophagic cells and their phagocytosis are crucial for inflammasome activation in macrophages

Gizem Ayna, Dmitri Krysko UGent, Agnieszka Kaczmarek UGent, Goran Petrovski, Peter Vandenabeele UGent and László Fésüs (2012) PLOS ONE. 7(6).
abstract
Pathogen-activated and damage-associated molecular patterns activate the inflammasome in macrophages. We report that mouse macrophages release IL-1 beta while co-incubated with pro-B (Ba/F3) cells dying, as a result of IL-3 withdrawal, by apoptosis with autophagy, but not when they are co-incubated with living, apoptotic, necrotic or necrostatin-1 treated cells. NALP3-deficient macrophages display reduced IL-1b secretion, which is also inhibited in macrophages deficient in caspase-1 or pre-treated with its inhibitor. This finding demonstrates that the inflammasome is activated during phagocytosis of dying autophagic cells. We show that activation of NALP3 depends on phagocytosis of dying cells, ATP release through pannexin-1 channels of dying autophagic cells, P2X7 purinergic receptor activation, and on consequent potassium efflux. Dying autophagic Ba/F3 cells injected intraperitoneally in mice recruit neutrophils and thereby induce acute inflammation. These findings demonstrate that NALP3 performs key upstream functions in inflammasome activation in mouse macrophages engulfing dying autophagic cells, and that these functions lead to pro-inflammatory responses.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
CALRETICULIN EXPOSURE, P2X(7) RECEPTOR, NALP3 INFLAMMASOME, IMMUNE-RESPONSES, INNATE IMMUNITY, DEATH, APOPTOSIS, MECHANISMS, IL-1-BETA, POTASSIUM
journal title
PLOS ONE
PLoS One
volume
7
issue
6
article_number
e40069
pages
14 pages
Web of Science type
Article
Web of Science id
000305892100194
JCR category
MULTIDISCIPLINARY SCIENCES
JCR impact factor
3.73 (2012)
JCR rank
7/56 (2012)
JCR quartile
1 (2012)
ISSN
1932-6203
DOI
10.1371/journal.pone.0040069
project
Ghent researchers on unfolded proteins in inflammatory disease (GROUP-ID)
project
Ghent researchers on unfolded proteins in inflammatory disease (GROUP-ID)
language
English
UGent publication?
yes
classification
A1
copyright statement
I have retained and own the full copyright for this publication
id
2968159
handle
http://hdl.handle.net/1854/LU-2968159
date created
2012-08-06 12:43:24
date last changed
2014-05-12 11:00:55
@article{2968159,
  abstract     = {Pathogen-activated and damage-associated molecular patterns activate the inflammasome in macrophages. We report that mouse macrophages release IL-1 beta while co-incubated with pro-B (Ba/F3) cells dying, as a result of IL-3 withdrawal, by apoptosis with autophagy, but not when they are co-incubated with living, apoptotic, necrotic or necrostatin-1 treated cells. NALP3-deficient macrophages display reduced IL-1b secretion, which is also inhibited in macrophages deficient in caspase-1 or pre-treated with its inhibitor. This finding demonstrates that the inflammasome is activated during phagocytosis of dying autophagic cells. We show that activation of NALP3 depends on phagocytosis of dying cells, ATP release through pannexin-1 channels of dying autophagic cells, P2X7 purinergic receptor activation, and on consequent potassium efflux. Dying autophagic Ba/F3 cells injected intraperitoneally in mice recruit neutrophils and thereby induce acute inflammation. These findings demonstrate that NALP3 performs key upstream functions in inflammasome activation in mouse macrophages engulfing dying autophagic cells, and that these functions lead to pro-inflammatory responses.},
  articleno    = {e40069},
  author       = {Ayna, Gizem and Krysko, Dmitri and Kaczmarek, Agnieszka and Petrovski, Goran and Vandenabeele, Peter and F{\'e}s{\"u}s, L{\'a}szl{\'o}},
  issn         = {1932-6203},
  journal      = {PLOS ONE},
  keyword      = {CALRETICULIN EXPOSURE,P2X(7) RECEPTOR,NALP3 INFLAMMASOME,IMMUNE-RESPONSES,INNATE IMMUNITY,DEATH,APOPTOSIS,MECHANISMS,IL-1-BETA,POTASSIUM},
  language     = {eng},
  number       = {6},
  pages        = {14},
  title        = {ATP release from dying autophagic cells and their phagocytosis are crucial for inflammasome activation in macrophages},
  url          = {http://dx.doi.org/10.1371/journal.pone.0040069},
  volume       = {7},
  year         = {2012},
}

Chicago
Ayna, Gizem, Dmitri Krysko, Agnieszka Kaczmarek, Goran Petrovski, Peter Vandenabeele, and László Fésüs. 2012. “ATP Release from Dying Autophagic Cells and Their Phagocytosis Are Crucial for Inflammasome Activation in Macrophages.” Plos One 7 (6).
APA
Ayna, G., Krysko, D., Kaczmarek, A., Petrovski, G., Vandenabeele, P., & Fésüs, L. (2012). ATP release from dying autophagic cells and their phagocytosis are crucial for inflammasome activation in macrophages. PLOS ONE, 7(6).
Vancouver
1.
Ayna G, Krysko D, Kaczmarek A, Petrovski G, Vandenabeele P, Fésüs L. ATP release from dying autophagic cells and their phagocytosis are crucial for inflammasome activation in macrophages. PLOS ONE. 2012;7(6).
MLA
Ayna, Gizem, Dmitri Krysko, Agnieszka Kaczmarek, et al. “ATP Release from Dying Autophagic Cells and Their Phagocytosis Are Crucial for Inflammasome Activation in Macrophages.” PLOS ONE 7.6 (2012): n. pag. Print.