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Neutrophilic NLRP3 inflammasome-dependent IL-1β secretion regulates the γδT17 cell response in respiratory bacterial infections

M Hassane, Dieter Demon UGent, D Soulard, J Fontaine, LE Keller, EC Patin, R Porte, I Prinz, B Ryffel, A Kadioglu, et al. (2017) MUCOSAL IMMUNOLOGY. 10(4). p.1056-1068
abstract
Traditionally regarded as simple foot soldiers of the innate immune response limited to the eradication of pathogens, neutrophils recently emerged as more complex cells endowed with a set of immunoregulatory functions. Using a model of invasive pneumococcal disease, we highlighted an unexpected key role for neutrophils as accessory cells in innate interleukin (IL)-17A production by lung resident V gamma 6V delta 1 (+) Tcells via nucleotide-binding oligomerization domain receptor, pyrin-containing 3 (NLRP3) inflammasome-dependent IL-1 beta secretion. In vivo activation of the NLRP3 inflammasome in neutrophils required both host-derived and bacterial-derived signals. Elaborately, it relies on (i) alveolar macrophage-secreted TNF-alpha for priming and (ii) subsequent exposure to bacterial pneumolysin for activation. Interestingly, this mechanism can be translated to human neutrophils. Our work revealed the cellular and molecular dynamic events leading to gamma delta T17 cell activation, and highlighted for the first time the existence of a fully functional NLRP3 inflammasome in lung neutrophils. This immune axis thus regulates the development of a protective host response to respiratory bacterial infections.
Please use this url to cite or link to this publication:
author
organization
alternative title
Neutrophilic NLRP3 inflammasome-dependent IL-1 beta secretion regulates the gamma delta T17 cell response in respiratory bacterial infections
year
type
journalArticle (original)
publication status
published
subject
keyword
DELTA T-CELLS, PNEUMONIAE LUNG INFECTION, STREPTOCOCCUS-PNEUMONIAE, PNEUMOCOCCAL PNEUMONIA, SERINE PROTEASES, TNF-ALPHA, DISEASE, ACTIVATION, ATP, COLONIZATION
journal title
MUCOSAL IMMUNOLOGY
Mucosal Immunol.
volume
10
issue
4
pages
1056 - 1068
Web of Science type
Article
Web of Science id
000403479300019
ISSN
1933-0219
1935-3456
DOI
10.1038/mi.2016.113
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
8525791
handle
http://hdl.handle.net/1854/LU-8525791
date created
2017-06-29 14:54:13
date last changed
2017-09-26 10:51:49
@article{8525791,
  abstract     = {Traditionally regarded as simple foot soldiers of the innate immune response limited to the eradication of pathogens, neutrophils recently emerged as more complex cells endowed with a set of immunoregulatory functions. Using a model of invasive pneumococcal disease, we highlighted an unexpected key role for neutrophils as accessory cells in innate interleukin (IL)-17A production by lung resident V gamma 6V delta 1 (+) Tcells via nucleotide-binding oligomerization domain receptor, pyrin-containing 3 (NLRP3) inflammasome-dependent IL-1 beta secretion. In vivo activation of the NLRP3 inflammasome in neutrophils required both host-derived and bacterial-derived signals. Elaborately, it relies on (i) alveolar macrophage-secreted TNF-alpha for priming and (ii) subsequent exposure to bacterial pneumolysin for activation. Interestingly, this mechanism can be translated to human neutrophils. Our work revealed the cellular and molecular dynamic events leading to gamma delta T17 cell activation, and highlighted for the first time the existence of a fully functional NLRP3 inflammasome in lung neutrophils. This immune axis thus regulates the development of a protective host response to respiratory bacterial infections.},
  author       = {Hassane, M and Demon, Dieter and Soulard, D and Fontaine, J and Keller, LE and Patin, EC and Porte, R and Prinz, I and Ryffel, B and Kadioglu, A and Veening, J-W and Sirard, J-C and Faveeuw, C and Lamkanfi, Mohamed and Trottein, F and Paget, C},
  issn         = {1933-0219},
  journal      = {MUCOSAL IMMUNOLOGY},
  keyword      = {DELTA T-CELLS,PNEUMONIAE LUNG INFECTION,STREPTOCOCCUS-PNEUMONIAE,PNEUMOCOCCAL PNEUMONIA,SERINE PROTEASES,TNF-ALPHA,DISEASE,ACTIVATION,ATP,COLONIZATION},
  language     = {eng},
  number       = {4},
  pages        = {1056--1068},
  title        = {Neutrophilic NLRP3 inflammasome-dependent IL-1\ensuremath{\beta} secretion regulates the \ensuremath{\gamma}\ensuremath{\delta}T17 cell response in respiratory bacterial infections},
  url          = {http://dx.doi.org/10.1038/mi.2016.113},
  volume       = {10},
  year         = {2017},
}

Chicago
Hassane, M, Dieter Demon, D Soulard, J Fontaine, LE Keller, EC Patin, R Porte, et al. 2017. “Neutrophilic NLRP3 Inflammasome-dependent IL-1β Secretion Regulates the γδT17 Cell Response in Respiratory Bacterial Infections.” Mucosal Immunology 10 (4): 1056–1068.
APA
Hassane, M., Demon, D., Soulard, D., Fontaine, J., Keller, L., Patin, E., Porte, R., et al. (2017). Neutrophilic NLRP3 inflammasome-dependent IL-1β secretion regulates the γδT17 cell response in respiratory bacterial infections. MUCOSAL IMMUNOLOGY, 10(4), 1056–1068.
Vancouver
1.
Hassane M, Demon D, Soulard D, Fontaine J, Keller L, Patin E, et al. Neutrophilic NLRP3 inflammasome-dependent IL-1β secretion regulates the γδT17 cell response in respiratory bacterial infections. MUCOSAL IMMUNOLOGY. 2017;10(4):1056–68.
MLA
Hassane, M, Dieter Demon, D Soulard, et al. “Neutrophilic NLRP3 Inflammasome-dependent IL-1β Secretion Regulates the γδT17 Cell Response in Respiratory Bacterial Infections.” MUCOSAL IMMUNOLOGY 10.4 (2017): 1056–1068. Print.