NLRP3 inflammasome activation in hepatocytes results in pyroptotic cell death, release of NLRP3 particles and liver fibrosis

2018 ◽  
Vol 68 ◽  
pp. S31-S32
Author(s):  
S. Schuster ◽  
F.A. Guerra ◽  
C.D. Johnson ◽  
C.J. Calvente ◽  
D. Povero ◽  
...  
Keyword(s):  
Cell Death ◽  
Liver Fibrosis ◽  
Nlrp3 Inflammasome ◽  
Inflammasome Activation ◽  
Nlrp3 Inflammasome Activation

scholarly journals MyD88 in Macrophages Enhances Liver Fibrosis by Activation of NLRP3 Inflammasome in HSCs

2021 ◽  
Vol 22 (22) ◽  
pp. 12413
Author(s):  
Shuang Ge ◽  
Wei Yang ◽  
Haiqiang Chen ◽  
Qi Yuan ◽  
Shi Liu ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Nlrp3 Inflammasome ◽  
Inflammatory Cell ◽  
Myeloid Cells ◽  
Inflammasome Activation ◽  
Potential Candidate ◽  
Pyrin Domain ◽  
Nlrp3 Inflammasome Activation ◽  
Candidate Target

Chronic liver disease mediated by the activation of hepatic stellate cells (HSCs) leads to liver fibrosis. The signal adaptor MyD88 of Toll-like receptor (TLR) signaling is involved during the progression of liver fibrosis. However, the specific role of MyD88 in myeloid cells in liver fibrosis has not been thoroughly investigated. In this study, we used a carbon tetrachloride (CCl4)-induced mouse fibrosis model in which MyD88 was selectively depleted in myeloid cells. MyD88 deficiency in myeloid cells attenuated liver fibrosis in mice and decreased inflammatory cell infiltration. Furthermore, deficiency of MyD88 in macrophages inhibits the secretion of CXC motif chemokine 2 (CXCL2), which restrains the activation of HSCs characterized by NLR Family Pyrin Domain Containing 3 (NLRP3) inflammasome activation. Moreover, targeting CXCL2 by CXCR2 inhibitors attenuated the activation of HSCs and reduced liver fibrosis. Thus, MyD88 may represent a potential candidate target for the prevention and treatment of liver fibrosis.

scholarly journals IRF8 Regulates Gram-Negative Bacteria–Mediated NLRP3 Inflammasome Activation and Cell Death

2020 ◽  
Vol 204 (9) ◽  
pp. 2514-2522 ◽  
Author(s):  
Rajendra Karki ◽  
Ein Lee ◽  
Bhesh R. Sharma ◽  
Balaji Banoth ◽  
Thirumala-Devi Kanneganti
Keyword(s):  
Cell Death ◽  
Nlrp3 Inflammasome ◽  
Inflammasome Activation ◽  
Gram Negative Bacteria ◽  
Gram Negative ◽  
Nlrp3 Inflammasome Activation

scholarly journals ZBP1: A STARGᐰTE to decode the biology of Z-nucleic acids in disease

2020 ◽  
Vol 217 (7) ◽  
Author(s):  
Sannula Kesavardhana ◽  
Thirumala-Devi Kanneganti
Keyword(s):  
Cell Death ◽  
Nucleic Acids ◽  
Inflammatory Disease ◽  
Nlrp3 Inflammasome ◽  
Inflammasome Activation ◽  
Nlrp3 Inflammasome Activation ◽  
Specific Ligand

ZBP1 triggers NLRP3 inflammasome activation/pyroptosis, apoptosis, and necroptosis; the specific ligand for ZBP1 activation remains ambiguous. Recent studies, including Devos et al. in this issue of JEM (https://doi.org/10.1084/jem.20191913), collectively suggest that ZBP1 sensing Z-nucleic acids is critical for cell death/inflammatory disease.

scholarly journals NLRP3 inflammasome activation drives bystander cone photoreceptor cell death in a P23H rhodopsin model of retinal degeneration

2016 ◽  
Vol 25 (8) ◽  
pp. 1501-1516 ◽  
Author(s):  
Ishaq A. Viringipurampeer ◽  
Andrew L. Metcalfe ◽  
Abu E. Bashar ◽  
Olena Sivak ◽  
Anat Yanai ◽  
...  
Keyword(s):  
Cell Death ◽  
Retinal Degeneration ◽  
Nlrp3 Inflammasome ◽  
Photoreceptor Cell ◽  
Inflammasome Activation ◽  
Cone Photoreceptor ◽  
Nlrp3 Inflammasome Activation

scholarly journals Lytic cell death induced by melittin bypasses pyroptosis but induces NLRP3 inflammasome activation and IL-1β release

2017 ◽  
Vol 8 (8) ◽  
pp. e2984-e2984 ◽  
Author(s):  
Fátima Martín-Sánchez ◽  
Juan José Martínez-García ◽  
María Muñoz-García ◽  
Miriam Martínez-Villanueva ◽  
José A Noguera-Velasco ◽  
...  
Keyword(s):  
Cell Death ◽  
Nlrp3 Inflammasome ◽  
Inflammasome Activation ◽  
Nlrp3 Inflammasome Activation

scholarly journals NLRP3 Inflammasome Activation-Mediated Pyroptosis Aggravates Myocardial Ischemia/Reperfusion Injury in Diabetic Rats

2017 ◽  
Vol 2017 ◽  
pp. 1-17 ◽  
Author(s):  
Zhen Qiu ◽  
Shaoqing Lei ◽  
Bo Zhao ◽  
Yang Wu ◽  
Wating Su ◽  
...  
Keyword(s):  
Cell Death ◽  
Myocardial Ischemia ◽  
Nlrp3 Inflammasome ◽  
Ischemia Reperfusion ◽  
Diabetic Rats ◽  
Receptor Protein ◽  
Inflammasome Activation ◽  
Myocardial Infarct Size ◽  
Nlrp3 Inflammasome Activation ◽  
Myocardial Ischemia Reperfusion

The reactive oxygen species- (ROS-) induced nod-like receptor protein-3 (NLRP3) inflammasome triggers sterile inflammatory responses and pyroptosis, which is a proinflammatory form of programmed cell death initiated by the activation of inflammatory caspases. NLRP3 inflammasome activation plays an important role in myocardial ischemia/reperfusion (MI/R) injury. Our present study investigated whether diabetes aggravated MI/R injury through NLRP3 inflammasome-mediated pyroptosis. Type 1 diabetic rat model was established by intraperitoneal injection of streptozotocin (60 mg/kg). MI/R was induced by ligating the left anterior descending artery (LAD) for 30 minutes followed by 2 h reperfusion. H9C2 cardiomyocytes were exposed to high glucose (HG, 30 mM) conditions and hypoxia/reoxygenation (H/R) stimulation. The myocardial infarct size, CK-MB, and LDH release in the diabetic rats subjected to MI/R were significantly higher than those in the nondiabetic rats, accompanied with increased NLRP3 inflammasome activation and increased pyroptosis. Inhibition of inflammasome activation with BAY11-7082 significantly decreased the MI/R injury.In vitrostudies showed similar effects, as BAY11-7082 or the ROS scavenger N-acetylcysteine, attenuated HG and H/R-induced H9C2 cell injury. In conclusion, hyperglycaemia-induced NLRP3 inflammasome activation may be a ROS-dependent process in pyroptotic cell death, and NLRP3 inflammasome-induced pyroptosis aggravates MI/R injury in diabetic rats.

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