scholarly journals SYK-CARD9 Signaling Axis Promotes Gut Fungi-Mediated Inflammasome Activation to Restrict Colitis and Colon Cancer

Immunity ◽  
2018 ◽  
Vol 49 (3) ◽  
pp. 515-530.e5 ◽  
Author(s):  
Ankit Malik ◽  
Deepika Sharma ◽  
R.K. Subbarao Malireddi ◽  
Clifford S. Guy ◽  
Ti-Cheng Chang ◽  
...  
2021 ◽  
Author(s):  
Lili Li ◽  
Xiaohui Zhu ◽  
Xingxing Chai ◽  
Xiaoyu Chen ◽  
Xiaohua Su ◽  
...  

Abstract Helicobacter pylori ( H. pylori ) is a major pathogenic factor for the development of gastric diseases including chronic gastritis and gastric cancer. Callicarpa nudiflora (CN), an air-dried leaves extract of Callicarpa nudiflora Hook. & Arn., has been found to exhibit a broad-spectrum antibacterial effect. In our study, we extracted the active ingredient from air-dried leaves of Callicarpa nudiflora, detected the effect of CN against H. pylori -infected GES-1 cells in vitro , and elucidated the underlying mechanism. GES-1 cells were cocultured with HPSS1 at MOI = 100:1 and treated with different concentrations of CN. Results indicated that CN not only significantly decreased cellular lactate dehydrogenase leakage, but also markedly attenuated H. pylori -induced cell apoptosis and ROS production in GSE-1 cells, therefore protecting gastric epithelial cells against injuries caused by H. pylori . CN also inhibited the secretions of inflammatory factors, such as tumor necrosis factor-α (TNF-α), IL-1β, IL-6 and IL-8. Furthermore, CN remarkably decreased the expression levels of NLRP3, PYCARD, active Caspase-1. In conclusion, CN exhibited highly efficient protective effect against H. pylori -induced gastritis and cell damage; Mechanismly, CN suppressed H. pylori -triggered inflammatory response and pyroptosis through depressing ROS production and NLRP3 inflammasome activation via ROS/NLRP3/IL-1β signaling axis.


Diabetes ◽  
2012 ◽  
Vol 61 (6) ◽  
pp. 1471-1478 ◽  
Author(s):  
S. Sun ◽  
S. Xia ◽  
Y. Ji ◽  
S. Kersten ◽  
L. Qi

2018 ◽  
Vol 78 (14) ◽  
pp. 3793-3808 ◽  
Author(s):  
Pit Ullmann ◽  
Fabien Rodriguez ◽  
Martine Schmitz ◽  
Steffen K. Meurer ◽  
Komal Qureshi-Baig ◽  
...  

2020 ◽  
Vol 205 (8) ◽  
pp. 2265-2275
Author(s):  
Daniel Swafford ◽  
Arulkumaran Shanmugam ◽  
Punithavathi Ranganathan ◽  
Indumathi Manoharan ◽  
Mohamed S. Hussein ◽  
...  

2019 ◽  
Vol 217 (3) ◽  
Author(s):  
R.K. Subbarao Malireddi ◽  
Prajwal Gurung ◽  
Sannula Kesavardhana ◽  
Parimal Samir ◽  
Amanda Burton ◽  
...  

RIPK1 kinase activity has been shown to be essential to driving pyroptosis, apoptosis, and necroptosis. However, here we show a kinase activity–independent role for RIPK1 in these processes using a model of TLR priming in a TAK1-deficient setting to mimic pathogen-induced priming and inhibition. TLR priming of TAK1-deficient macrophages triggered inflammasome activation, including the activation of caspase-8 and gasdermin D, and the recruitment of NLRP3 and ASC into a novel RIPK1 kinase activity–independent cell death complex to drive pyroptosis and apoptosis. Furthermore, we found fully functional RIPK1 kinase activity–independent necroptosis driven by the RIPK3–MLKL pathway in TAK1-deficient macrophages. In vivo, TAK1 inactivation resulted in RIPK3–caspase-8 signaling axis–driven myeloid proliferation and a severe sepsis-like syndrome. Overall, our study highlights a previously unknown mechanism for RIPK1 kinase activity–independent inflammasome activation and pyroptosis, apoptosis, and necroptosis (PANoptosis) that could be targeted for treatment of TAK1-associated myeloid proliferation and sepsis.


2016 ◽  
Vol 14 (5) ◽  
pp. 4559-4566 ◽  
Author(s):  
Lin Yang ◽  
Yanqing Liu ◽  
Mei Wang ◽  
Yayun Qian ◽  
Xiaoyun Dong ◽  
...  

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