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

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Neutrophilic NLRP3 inflammasome-dependent IL-1β secretion regulates the γδT17 cell response in respiratory bacterial infections. / Hassane, M; Demon, D; Soulard, D; Fontaine, J; Keller, L E; Patin, E C; Porte, R; Prinz, I; Ryffel, B; Kadioglu, A; Veening, J-W; Sirard, J-C; Faveeuw, C; Lamkanfi, M; Trottein, F; Paget, C.

In: MUCOSAL IMMUNOL, Vol. 10, No. 4, 07.2017, p. 1056-1068.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Hassane, M, Demon, D, Soulard, D, Fontaine, J, Keller, LE, Patin, EC, Porte, R, Prinz, I, Ryffel, B, Kadioglu, A, Veening, J-W, Sirard, J-C, Faveeuw, C, Lamkanfi, M, Trottein, F & Paget, C 2017, 'Neutrophilic NLRP3 inflammasome-dependent IL-1β secretion regulates the γδT17 cell response in respiratory bacterial infections', MUCOSAL IMMUNOL, vol. 10, no. 4, pp. 1056-1068. https://doi.org/10.1038/mi.2016.113

APA

Hassane, M., Demon, D., Soulard, D., Fontaine, J., Keller, L. E., Patin, E. C., Porte, R., Prinz, I., Ryffel, B., Kadioglu, A., Veening, J-W., Sirard, J-C., Faveeuw, C., Lamkanfi, M., Trottein, F., & Paget, C. (2017). Neutrophilic NLRP3 inflammasome-dependent IL-1β secretion regulates the γδT17 cell response in respiratory bacterial infections. MUCOSAL IMMUNOL, 10(4), 1056-1068. https://doi.org/10.1038/mi.2016.113

Vancouver

Hassane M, Demon D, Soulard D, Fontaine J, Keller LE, Patin EC et al. Neutrophilic NLRP3 inflammasome-dependent IL-1β secretion regulates the γδT17 cell response in respiratory bacterial infections. MUCOSAL IMMUNOL. 2017 Jul;10(4):1056-1068. https://doi.org/10.1038/mi.2016.113

Bibtex

@article{a46a8f99dae24393b0abba1f5862f8e2,
title = "Neutrophilic NLRP3 inflammasome-dependent IL-1β secretion regulates the γδT17 cell response in respiratory bacterial infections",
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 Vγ6Vδ1+ T cells via nucleotide-binding oligomerization domain receptor, pyrin-containing 3 (NLRP3) inflammasome-dependent IL-1β 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-α 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 γδT17 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.",
keywords = "Animals, Bacterial Proteins/immunology, Cells, Cultured, Disease Models, Animal, Humans, Inflammasomes/metabolism, Interleukin-17/genetics, Interleukin-1beta/metabolism, Macrophages, Alveolar/immunology, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, NLR Family, Pyrin Domain-Containing 3 Protein/genetics, Neutrophils/immunology, Pneumococcal Infections/immunology, Receptors, Antigen, T-Cell, gamma-delta/genetics, Respiratory Tract Infections/immunology, Streptococcus pneumoniae/immunology, Streptolysins/immunology, Th17 Cells/immunology, Tumor Necrosis Factor-alpha/metabolism",
author = "M Hassane and D Demon and D Soulard and J Fontaine and Keller, {L E} and Patin, {E C} and R Porte and I Prinz and B Ryffel and A Kadioglu and J-W Veening and J-C Sirard and C Faveeuw and M Lamkanfi and F Trottein and C Paget",
year = "2017",
month = jul,
doi = "10.1038/mi.2016.113",
language = "English",
volume = "10",
pages = "1056--1068",
journal = "MUCOSAL IMMUNOL",
issn = "1933-0219",
publisher = "NATURE PUBLISHING GROUP",
number = "4",

}

RIS

TY - JOUR

T1 - Neutrophilic NLRP3 inflammasome-dependent IL-1β secretion regulates the γδT17 cell response in respiratory bacterial infections

AU - Hassane, M

AU - Demon, D

AU - Soulard, D

AU - Fontaine, J

AU - Keller, L E

AU - Patin, E C

AU - Porte, R

AU - Prinz, I

AU - Ryffel, B

AU - Kadioglu, A

AU - Veening, J-W

AU - Sirard, J-C

AU - Faveeuw, C

AU - Lamkanfi, M

AU - Trottein, F

AU - Paget, C

PY - 2017/7

Y1 - 2017/7

N2 - 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 Vγ6Vδ1+ T cells via nucleotide-binding oligomerization domain receptor, pyrin-containing 3 (NLRP3) inflammasome-dependent IL-1β 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-α 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 γδT17 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.

AB - 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 Vγ6Vδ1+ T cells via nucleotide-binding oligomerization domain receptor, pyrin-containing 3 (NLRP3) inflammasome-dependent IL-1β 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-α 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 γδT17 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.

KW - Animals

KW - Bacterial Proteins/immunology

KW - Cells, Cultured

KW - Disease Models, Animal

KW - Humans

KW - Inflammasomes/metabolism

KW - Interleukin-17/genetics

KW - Interleukin-1beta/metabolism

KW - Macrophages, Alveolar/immunology

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - NLR Family, Pyrin Domain-Containing 3 Protein/genetics

KW - Neutrophils/immunology

KW - Pneumococcal Infections/immunology

KW - Receptors, Antigen, T-Cell, gamma-delta/genetics

KW - Respiratory Tract Infections/immunology

KW - Streptococcus pneumoniae/immunology

KW - Streptolysins/immunology

KW - Th17 Cells/immunology

KW - Tumor Necrosis Factor-alpha/metabolism

U2 - 10.1038/mi.2016.113

DO - 10.1038/mi.2016.113

M3 - SCORING: Journal article

C2 - 28051086

VL - 10

SP - 1056

EP - 1068

JO - MUCOSAL IMMUNOL

JF - MUCOSAL IMMUNOL

SN - 1933-0219

IS - 4

ER -