TY - JOUR
T1 - Group 2 innate lymphoid cells protect lung endothelial cells from pyroptosis in sepsis article
AU - Lai, Dengming
AU - Tang, Jing
AU - Chen, Linsong
AU - Fan, Erica K.
AU - Scott, Melanie J.
AU - Li, Yuehua
AU - Billiar, Timothy R.
AU - Wilson, Mark A.
AU - Fang, Xiangming
AU - Shu, Qiang
AU - Fan, Jie
N1 - Funding Information:
This work was supported by the National Institutes of Health Grant R01-HL-079669 (J.F. and M.A.W.), National Institutes of Health Grant R56-HL-123882 (J. F.), National Institutes of Health Grant R01HL076179-09 (J.F.), VA Merit Award 1I01BX002729 (J.F.), National Natural Science Foundation of China 81470262 (J. F.), Zhejiang Provincial Program for the Cultivation of High-level Innovative Health talents 2016-6 (Q.S.), the National Natural Science Foundation of China 81671956 (Q.S.), and National Institutes of Health Grant R01GM102146 (M.J.S).
Publisher Copyright:
© 2018 The Author(s).
PY - 2018/3/1
Y1 - 2018/3/1
N2 - Group 2 innate lymphoid cells (ILC2) are one of three subgroups of innate lymphoid cells (ILC1, ILC2, and ILC3), and the major ILC population detected in the lungs. The function of ILC2 in the regulation of lung inflammation remains unclear. In the current study, we explored an important role of ILC2 in protecting lung endothelial cell (EC) from pyroptosis in sepsis-induced acute lung inflammation and the underlying mechanism. Using a cecal ligation and puncture (CLP) mouse sepsis model, we demonstrated that IL-33, which is released in response to sepsis, acting through its receptor ST2 mediates ILC2 expansion in the lungs. We further showed that the increased ILC2 in the lungs secrete IL-9, which in turn prevents lung EC from undergoing pyroptosis, a pro-inflammatory cell death form, by attenuating caspase-1 activation. These findings suggest a previously unidentified innate pathway that negatively regulates lung inflammation following sepsis.
AB - Group 2 innate lymphoid cells (ILC2) are one of three subgroups of innate lymphoid cells (ILC1, ILC2, and ILC3), and the major ILC population detected in the lungs. The function of ILC2 in the regulation of lung inflammation remains unclear. In the current study, we explored an important role of ILC2 in protecting lung endothelial cell (EC) from pyroptosis in sepsis-induced acute lung inflammation and the underlying mechanism. Using a cecal ligation and puncture (CLP) mouse sepsis model, we demonstrated that IL-33, which is released in response to sepsis, acting through its receptor ST2 mediates ILC2 expansion in the lungs. We further showed that the increased ILC2 in the lungs secrete IL-9, which in turn prevents lung EC from undergoing pyroptosis, a pro-inflammatory cell death form, by attenuating caspase-1 activation. These findings suggest a previously unidentified innate pathway that negatively regulates lung inflammation following sepsis.
UR - http://www.scopus.com/inward/record.url?scp=85042927372&partnerID=8YFLogxK
U2 - 10.1038/s41419-018-0412-5
DO - 10.1038/s41419-018-0412-5
M3 - Article
C2 - 29511181
AN - SCOPUS:85042927372
SN - 2041-4889
VL - 9
JO - Cell Death and Disease
JF - Cell Death and Disease
IS - 3
M1 - 369
ER -