Tumor necrosis factor-alpha and interferon-gamma induce inflammasome-mediated corneal endothelial cell death

2021 ◽  
Vol 207 ◽  
pp. 108574
Author(s):  
Angela Gomez ◽  
Andres Serrano ◽  
Enrique Salero ◽  
Arianna Tovar ◽  
Guillermo Amescua ◽  
...  
2003 ◽  
Vol 64 (6) ◽  
pp. 734-735 ◽  
Author(s):  
Simon V. Skurkovich ◽  
Yu A. Aleksandrovsky ◽  
Vladimir P. Chekhonin ◽  
Igor A. Ryabukhin ◽  
Konstantin O. Chakhava ◽  
...  

Pathobiology ◽  
1994 ◽  
Vol 62 (3) ◽  
pp. 120-126 ◽  
Author(s):  
Thomas Chang-Yao Tsao ◽  
Weijia Xia ◽  
Gary M. Rodberg ◽  
Clare E. Pinto ◽  
Richard L. Kradin

1995 ◽  
Vol 269 (2) ◽  
pp. G297-G304 ◽  
Author(s):  
J. H. Wang ◽  
H. P. Redmond ◽  
R. W. Watson ◽  
D. Bouchier-Hayes

The occurrence of acute hepatic failure during systemic inflammatory response syndrome (SIRS) is related to the extent of hepatocyte (HC) damage and cell death resulting from necrosis or apoptosis. We hypothesized that proinflammatory mediators such as lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF-alpha) can, either directly or indirectly through neutrophil (PMN) and Kupffer cell (KC) activation, induce HC damage and cell death, and that the mechanism is cellular necrosis rather than apoptosis. The results in this study demonstrated that LPS and TNF-alpha alone and in combination are directly cytotoxic to cultured rat HC as indicated by the hepatocellular enzyme release and HC necrosis. However, LPS and TNF-alpha, in the presence of sodium arsenite (a heat shock inducer), were unable to induce HC apoptosis. Both KC and PMN activated by either LPS or TNF-alpha induced significant hepatocellular enzyme release and HC necrosis, which was dependent on the ratio of KC and PMN to HC. It is concluded that LPS and TNF-alpha may play a central role in the development of acute hepatic failure after severe trauma and sepsis by directly or indirectly inducing HC necrosis rather than apoptosis.


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