https://scholars.lib.ntu.edu.tw/handle/123456789/190849
標題: | Capsular Polysaccharide Is Involved in NLRP3 Inflammasome Activation by Klebsiella pneumoniae Serotype K1 | 作者: | Hua, Kuo-Feng Yang, Feng-Ling Chiu, Hsiao-Wen Chou, Ju-Ching Dong, Wei-Chih Lin, Chien-Nan Lin, Chai-Yi JIN-TOWN WANG Li, Lan-Hui Chiu, Huan-Wen Chiu, Yi-Chich Wu, Shih-Hsiung McCormick, B. A. |
公開日期: | 2015 | 起(迄)頁: | 3396-3409 | 來源出版物: | Infection and Immunity | 摘要: | Klebsiella pneumoniae (strain 43816, K2 serotype) induces interleukin-1 beta (IL-1 beta) secretion, but neither the bacterial factor triggering the activation of these inflammasome-dependent responses nor whether they are mediated by NLRP3 or NLRC4 is known. In this study, we identified a capsular polysaccharide (K1-CPS) in K. pneumoniae (NTUH-K2044, K1 serotype), isolated from a primary pyogenic liver abscess (PLA K. pneumoniae), as the Klebsiella factor that induces IL-1 beta secretion in an NLRP3-, ASC-, and caspase-1-dependent manner in macrophages. K1-CPS induced NLRP3 inflammasome activation through reactive oxygen species (ROS) generation, mitogen-activated protein kinase phosphorylation, and NF-kappa B activation. Inhibition of both the mitochondrial membrane permeability transition and mitochondrial ROS generation inhibited K1-CPS-mediated NLRP3 inflammasome activation. Furthermore, IL-1 beta secretion in macrophages infected with PLA K. pneumoniae was shown to depend on NLRP3 but also on NLRC4 and TLR4. In macrophages infected with a K1-CPS deficiency mutant, an lipopolysaccharide (LPS) deficiency mutant, or K1-CPS and LPS double mutants, IL-1 beta secretion levels were lower than those in cells infected with wild-type PLA K. pneumoniae. Our findings indicate that K1-CPS is one of the Klebsiella factors of PLA K. pneumoniae that induce IL-1 beta secretion through the NLRP3 inflammasome. |
URI: | http://ntur.lib.ntu.edu.tw//handle/246246/270683 | DOI: | 10.1128/IAI.00125-15 |
顯示於: | 醫學系 |
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