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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
toll like receptor 2
tumor necrosis factor
animal experiment
animal tissue
antiinflammatory activity
bacterial infection
controlled study
flow cytometry
gene sequence
genetic transcription
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.
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
ISSN: 16643224
DOI: 10.3389/fimmu.2018.01445
Rights: Attribution 4.0 International
Appears in Collections:Staff Publications

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