Rossol, M., Pierer, M., Raulien, N., Quandt, D., Meusch, U., Rothe, K., Schubert, K., Schöneberg, T., Schaefer, M., Krügel, U., Smajilovic, S., Bräuner-Osborne, H., Baerwald, C., & Wagner, U. (2012). Extracellular Ca2+ is a danger signal activating the NLRP3 inflammasome through G protein-coupled calcium sensing receptors. Nature Communications, 3, 1329. https://doi.org/10.1038/ncomms2339
Extracellular Ca2+ is a danger signal activating the NLRP3 inflammasome through G protein-coupled calcium sensing receptors. / Rossol, Manuela; Pierer, Matthias; Raulien, Nora et al.
In:
Nature Communications, Vol. 3, 2012, p. 1329.
Research output: Contribution to journal › Journal article › Research › peer-review
Rossol, M, Pierer, M, Raulien, N, Quandt, D, Meusch, U, Rothe, K, Schubert, K, Schöneberg, T, Schaefer, M, Krügel, U, Smajilovic, S, Bräuner-Osborne, H, Baerwald, C & Wagner, U 2012, 'Extracellular Ca2+ is a danger signal activating the NLRP3 inflammasome through G protein-coupled calcium sensing receptors', Nature Communications, vol. 3, pp. 1329. https://doi.org/10.1038/ncomms2339
Rossol M, Pierer M, Raulien N, Quandt D, Meusch U, Rothe K et al. Extracellular Ca2+ is a danger signal activating the NLRP3 inflammasome through G protein-coupled calcium sensing receptors. Nature Communications. 2012;3:1329. doi: 10.1038/ncomms2339
Rossol, Manuela ; Pierer, Matthias ; Raulien, Nora et al. / Extracellular Ca2+ is a danger signal activating the NLRP3 inflammasome through G protein-coupled calcium sensing receptors. In: Nature Communications. 2012 ; Vol. 3. pp. 1329.
@article{0d795776c8234dd0a7d84aef0de142a3,
title = "Extracellular Ca2+ is a danger signal activating the NLRP3 inflammasome through G protein-coupled calcium sensing receptors",
abstract = "Activation of the NLRP3 inflammasome enables monocytes and macrophages to release high levels of interleukin-1β during inflammatory responses. Concentrations of extracellular calcium can increase at sites of infection, inflammation or cell activation. Here we show that increased extracellular calcium activates the NLRP3 inflammasome via stimulation of G protein-coupled calcium sensing receptors. Activation is mediated by signalling through the calcium-sensing receptor and GPRC6A via the phosphatidyl inositol/Ca2 pathway. The resulting increase in the intracellular calcium concentration triggers inflammasome assembly and Caspase-1 activation. We identified necrotic cells as one source for excess extracellular calcium triggering this activation. In vivo, increased calcium concentrations can amplify the inflammatory response in the mouse model of carrageenan-induced footpad swelling, and this effect was inhibited in GPRC6A -/- mice. Our results demonstrate that G-protein-coupled receptors can activate the inflammasome, and indicate that increased extracellular calcium has a role as a danger signal and amplifier of inflammation.",
author = "Manuela Rossol and Matthias Pierer and Nora Raulien and Dagmar Quandt and Undine Meusch and Kathrin Rothe and Kristin Schubert and Torsten Sch{\"o}neberg and Michael Schaefer and Ute Kr{\"u}gel and Sanela Smajilovic and Hans Br{\"a}uner-Osborne and Christoph Baerwald and Ulf Wagner",
note = "Article number: 1329",
year = "2012",
doi = "10.1038/ncomms2339",
language = "English",
volume = "3",
pages = "1329",
journal = "Nature Communications",
issn = "2041-1723",
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}
TY - JOUR
T1 - Extracellular Ca2+ is a danger signal activating the NLRP3 inflammasome through G protein-coupled calcium sensing receptors
AU - Rossol, Manuela
AU - Pierer, Matthias
AU - Raulien, Nora
AU - Quandt, Dagmar
AU - Meusch, Undine
AU - Rothe, Kathrin
AU - Schubert, Kristin
AU - Schöneberg, Torsten
AU - Schaefer, Michael
AU - Krügel, Ute
AU - Smajilovic, Sanela
AU - Bräuner-Osborne, Hans
AU - Baerwald, Christoph
AU - Wagner, Ulf
N1 - Article number: 1329
PY - 2012
Y1 - 2012
N2 - Activation of the NLRP3 inflammasome enables monocytes and macrophages to release high levels of interleukin-1β during inflammatory responses. Concentrations of extracellular calcium can increase at sites of infection, inflammation or cell activation. Here we show that increased extracellular calcium activates the NLRP3 inflammasome via stimulation of G protein-coupled calcium sensing receptors. Activation is mediated by signalling through the calcium-sensing receptor and GPRC6A via the phosphatidyl inositol/Ca2 pathway. The resulting increase in the intracellular calcium concentration triggers inflammasome assembly and Caspase-1 activation. We identified necrotic cells as one source for excess extracellular calcium triggering this activation. In vivo, increased calcium concentrations can amplify the inflammatory response in the mouse model of carrageenan-induced footpad swelling, and this effect was inhibited in GPRC6A -/- mice. Our results demonstrate that G-protein-coupled receptors can activate the inflammasome, and indicate that increased extracellular calcium has a role as a danger signal and amplifier of inflammation.
AB - Activation of the NLRP3 inflammasome enables monocytes and macrophages to release high levels of interleukin-1β during inflammatory responses. Concentrations of extracellular calcium can increase at sites of infection, inflammation or cell activation. Here we show that increased extracellular calcium activates the NLRP3 inflammasome via stimulation of G protein-coupled calcium sensing receptors. Activation is mediated by signalling through the calcium-sensing receptor and GPRC6A via the phosphatidyl inositol/Ca2 pathway. The resulting increase in the intracellular calcium concentration triggers inflammasome assembly and Caspase-1 activation. We identified necrotic cells as one source for excess extracellular calcium triggering this activation. In vivo, increased calcium concentrations can amplify the inflammatory response in the mouse model of carrageenan-induced footpad swelling, and this effect was inhibited in GPRC6A -/- mice. Our results demonstrate that G-protein-coupled receptors can activate the inflammasome, and indicate that increased extracellular calcium has a role as a danger signal and amplifier of inflammation.
U2 - 10.1038/ncomms2339
DO - 10.1038/ncomms2339
M3 - Journal article
C2 - 23271661
SN - 2041-1723
VL - 3
SP - 1329
JO - Nature Communications
JF - Nature Communications
ER -
