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Schistosoma egg antigens suppress LPS-induced inflammation in human IMR-90 cells by modulation of JAK/STAT1 signaling
Type
article
Resource
Journal of microbiology; immunology; and infection = Wei mian yu gan ran za zhi; 54(3); 501–513.
Date Issued
2021-06
Author(s)
Lee, Kang-Yun;Lee, Yi-Lin;Chiang, Ming-Hsiu;Wang, Hung-Yang;Chen, Chong-Yu;Lin, Chang-Hong;Chen, Ying-Chou;Fan, Chia-Kwung;Cheng, Po-Ching
Subjects
學科：分子寄生蟲暨熱帶疾病學科
期刊論文
Description
【112-2 升等】臺北醫學大學教師升等專門著作
職別：專任
送審等級：教授
著作送審
代表著作名稱：《Schistosoma egg antigens suppress LPS-induced inflammation in human IMR-90 cells by modulation of JAK/STAT1 signaling》
Copyright ? 2020. Published by Elsevier B.V.
Abstract
Background: The regulation of the balance between inflammatory and anti-inflammatory events during the treatment of pulmonary infection is very important. Soluble Schistosoma egg antigens (SEA) can effectively inhibit the expression of cytokines during hepatic acute inflammation. However; the mechanisms by which these proteins suppress the inflammatory responses in lung cells remain unclear. The purpose of this study was to investigate the ability of SEA to inhibit pulmonary inflammation.
Methods: The effects of SEA were investigated in LPS-treated lung IMR-90 cells. The involvement of the JAK/STAT-1 signaling pathway in these effects was evaluated by employing CBA assays; quantitative polymerase chain reaction; and western blotting experiments.
Results: Pretreatment of IMR-90 cells with appropriate concentrations of SEA protected cells against the cytotoxic effects of LPS-induced inflammation in a time-dependent manner. SEA pretreatment significantly attenuated the LPS-induced activation of the JAK/STAT1 signaling pathway; including the upregulation of JAK1/2 and STAT1; as well as the production of inflammatory cytokines. The level of phosphorylated STAT1 gradually declined in response to increasing concentrations of SEA. Based on these findings; we hypothesize that SEA-induced anti-inflammatory effects initiate with the downregulation of the IFN-γ-JAK-STAT1 signaling pathway; resulting in the attenuation of LPS-induced inflammation in IMR-90 cells.
Conclusion: Our study is the first to demonstrate the anti-inflammatory activity of SEA in an in vitro model of pulmonary inflammation; involving the modulation of JAK/STAT1 signaling. We propose SEA as potential therapeutic or preventive agents for the selective suppression of STAT1 and the control of inflammatory response in lung IMR-90 cells.
Methods: The effects of SEA were investigated in LPS-treated lung IMR-90 cells. The involvement of the JAK/STAT-1 signaling pathway in these effects was evaluated by employing CBA assays; quantitative polymerase chain reaction; and western blotting experiments.
Results: Pretreatment of IMR-90 cells with appropriate concentrations of SEA protected cells against the cytotoxic effects of LPS-induced inflammation in a time-dependent manner. SEA pretreatment significantly attenuated the LPS-induced activation of the JAK/STAT1 signaling pathway; including the upregulation of JAK1/2 and STAT1; as well as the production of inflammatory cytokines. The level of phosphorylated STAT1 gradually declined in response to increasing concentrations of SEA. Based on these findings; we hypothesize that SEA-induced anti-inflammatory effects initiate with the downregulation of the IFN-γ-JAK-STAT1 signaling pathway; resulting in the attenuation of LPS-induced inflammation in IMR-90 cells.
Conclusion: Our study is the first to demonstrate the anti-inflammatory activity of SEA in an in vitro model of pulmonary inflammation; involving the modulation of JAK/STAT1 signaling. We propose SEA as potential therapeutic or preventive agents for the selective suppression of STAT1 and the control of inflammatory response in lung IMR-90 cells.