Interleukin-37 suppresses ICAM-1 expression in parallel with NF-κB down-regulation following TLR2 activation of human coronary artery endothelial cells
Autor: | Yandan Xie, Xiangna Cai, Yuguang Li, Jilin Li, Xin Wang |
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Rok vydání: | 2016 |
Předmět: |
0301 basic medicine
ICAM-1 medicine.medical_treatment Immunology Down-Regulation Stimulation Inflammation Peptidoglycan NF-κB Proinflammatory cytokine 03 medical and health sciences chemistry.chemical_compound medicine Humans TLR2 Immunology and Allergy RNA Small Interfering Cells Cultured Interleukin-37 Pharmacology NF-kappa B Endothelial Cells Interleukin Atherosclerosis Intercellular Adhesion Molecule-1 Coronary Vessels Immunity Innate Toll-Like Receptor 2 Cell biology 030104 developmental biology Cytokine chemistry HCAECs medicine.symptom Interleukin-1 Signal Transduction |
Zdroj: | International Immunopharmacology. 38:26-30 |
ISSN: | 1567-5769 |
DOI: | 10.1016/j.intimp.2016.05.003 |
Popis: | Introduction The inflammatory receptor Toll-like receptors (TLRs) activation could induce endothelial inflammatory responses, which plays an important role in the development of many diseases including atherosclerosis. We already found that TLR2 activation of Peptidoglycan (PGN) stimulation could increase intercellular adhesion molecule-1 (ICAM-1) expression in HCAECs. Since anti-inflammatory cytokine interleukin (IL)-37 exhibits intra- and extracellular properties for suppressing innate inflammation, we want to investigate whether IL-37 suppresses ICAM-1 expression and this effect is in parallel with the inhibition of nuclear factor kappa B (NF-κB) activation upon PGN stimulation in HCAECs. Methods HCAECs were treated with IL-37-transfection plasmid or silent mRNA or nothing for 24 h, and we test IL-37 expression by immunoblotting. Same treatments prior to PGN stimulation (10 μg/ml), we analyzed the expression of ICAM-1 and NF-κB mRNA at 0, 30 min, 1 and 2 h by real-time PCR. ICAM-1 protein at 24 h and NF-κB activation at 0–2 h were measured by immunoblotting. Results IL-37 and silent IL-37 transfection change the expression of IL-37 protein. Stimulation of PGN increased both NF-κB activation and ICAM-1 expression at mRNA and protein level, but these inflammatory cytokines’ expression was significantly decreased in IL-37-transfection cells. Interestingly, both NF-κB activation and ICAM-1 expression were significantly increased when IL-37 was silent. Conclusions As an anti-inflammatory cytokine, IL-37 could decrease both NF-κB and ICAM-1 expression upon TLR2 activation in HCAECs. The suppressed effect of IL-37 on ICAM-1 may be due to its inhibition on NF-κB. |
Databáze: | OpenAIRE |
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