Please use this identifier to cite or link to this item: https://doi.org/10.3389/fimmu.2018.01445
Title: Anti-allergic inflammatory activity of interleukin-37 is mediated by novel signaling cascades in human eosinophils
Authors: Zhu, J
Dong, J
Ji, L
Jiang, P
Leung, T.F
Liu, D
Ng, L.G 
Tsang, M.S.-M
Jiao, D
Lam, C.W.-K
Wong, C.-K
Keywords: eotaxin
interleukin 13
interleukin 17
interleukin 1beta
interleukin 37
interleukin 4
interleukin 6
interleukin 8
monocyte chemotactic protein 1
peptidoglycan
RANTES
toll like receptor 2
tumor necrosis factor
animal experiment
animal tissue
antiinflammatory activity
Article
bacterial infection
bioinformatics
controlled study
eosinophil
female
flow cytometry
gene sequence
genetic transcription
histopathology
human
male
mouse
nonhuman
real time polymerase chain reaction
RNA sequence
signal transduction
Issue Date: 2018
Citation: Zhu, J, Dong, J, Ji, L, Jiang, P, Leung, T.F, Liu, D, Ng, L.G, Tsang, M.S.-M, Jiao, D, Lam, C.W.-K, Wong, C.-K (2018). Anti-allergic inflammatory activity of interleukin-37 is mediated by novel signaling cascades in human eosinophils. Frontiers in Immunology 9 (JUN) : 1445. ScholarBank@NUS Repository. https://doi.org/10.3389/fimmu.2018.01445
Rights: Attribution 4.0 International
Abstract: IL-1 family regulatory cytokine IL-37b can suppress innate immunity and inflammatory activity in inflammatory diseases. In this study, IL-37b showed remarkable in vitro suppression of inflammatory tumor necrosis factor-?, IL-1?, IL-6, CCL2, and CXCL8 production in the coculture of human primary eosinophils and human bronchial epithelial BEAS-2B cells with the stimulation of bacterial toll-like receptor-2 ligand peptidoglycan, while antagonizing the activation of intracellular nuclear factor-?B, PI3K-Akt, extracellular signal-regulated kinase 1/2, and suppressing the gene transcription of allergic inflammation-related PYCARD, S100A9, and CAMP as demonstrated by flow cytometry, RNA-sequencing, and bioinformatics. Results therefore elucidated the novel anti-inflammation-related molecular mechanisms mediated by IL-37b. Using the house dust mite (HDM)-induced humanized asthmatic NOD/SCID mice for preclinical study, intravenous administration of IL-37b restored the normal plasma levels of eosinophil activators CCL11 and IL-5, suppressed the elevated concentrations of Th2 and asthma-related cytokines IL-4, IL-6, and IL-13 and inflammatory IL-17, CCL5, and CCL11 in lung homogenate of asthmatic mice. Histopathological results of lung tissue illustrated that IL-37b could mitigate the enhanced mucus, eosinophil infiltration, thickened airway wall, and goblet cells. Together with similar findings using the ovalbumin- and HDM-induced allergic asthmatic mice further validated the therapeutic potential of IL-37b in allergic asthma. The above results illustrate the novel IL-37-mediated regulation of intracellular inflammation mechanism linking bacterial infection and the activation of human eosinophils and confirm the in vivo anti-inflammatory activity of IL-37b on human allergic asthma. © 2018 Zhu, Dong, Ji, Jiang, Leung, Liu, Ng, Tsang, Jiao, Lam and Wong.
Source Title: Frontiers in Immunology
URI: https://scholarbank.nus.edu.sg/handle/10635/178082
ISSN: 16643224
DOI: 10.3389/fimmu.2018.01445
Rights: Attribution 4.0 International
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