scholarly journals Probiotic Bacterium Prevents Cytokine-induced Apoptosis in Intestinal Epithelial Cells

2002 ◽  
Vol 277 (52) ◽  
pp. 50959-50965 ◽  
Author(s):  
Fang Yan ◽  
D. Brent Polk
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Probiotic Bacterium ◽  
Intestinal Epithelial ◽  
Induced Apoptosis

Sequential and rapid activation of select caspases during apoptosis of normal intestinal epithelial cells

1998 ◽  
Vol 274 (6) ◽  
pp. G1117-G1124 ◽  
Author(s):  
Johannes Grossmann ◽  
Susanne Mohr ◽  
Eduardo G. Lapetina ◽  
Claudio Fiocchi ◽  
Alan D. Levine
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Cysteine Proteases ◽  
Intestinal Epithelial ◽  
Caspase Activation ◽  
High Turnover ◽  
Sequential Activation ◽  
Caspase 6 ◽  
Caspase Substrate ◽  
Induced Apoptosis

Detachment-induced cell death (DICD) is considered to be one of the means by which intestinal epithelial cells (IEC) die of apoptosis as they reach the lumen and are shed. Caspases, a family of cysteine proteases, play a central role in initiating, amplifying, and executing apoptosis; however, the pattern of caspase activation in response to distinct apoptotic stimuli remains unknown. We investigated the kinetics of caspase activation during DICD in freshly isolated human IEC. DNA fragmentation is observed 90 min after detachment and is preceded by the sequential activation of preformed members of the CPP32 family of caspases. Activation of caspase 6 and cleavage of the endogenous caspase substrate poly(ADP-ribose) polymerase (EC 2.4.2.30 ) are detected within 15 min of detachment, 30–45 min before caspase 3 activation. Caspase 1 and caspase 10 are present as proenzymes, yet they remain inactive in response to this trigger of apoptosis. Human IEC are primed to rapidly undergo detachment-induced apoptosis involving the selective and sequential activation of preformed caspases. This study may enhance our understanding of physiological events occurring as IEC are shed. Their rapid apoptotic response to detachment may facilitate the high turnover of cells and ensure homeostasis in the intestinal epithelium.

Effects of Stearic Acid on Proliferation, Differentiation, Apoptosis, and Autophagy in Porcine Intestinal Epithelial Cells

2020 ◽  
Vol 20 (2) ◽  
pp. 157-166
Author(s):  
Yuan Yang ◽  
Jin Huang ◽  
Jianzhong Li ◽  
Huansheng Yang ◽  
Yulong Yin
Keyword(s):  
Cell Differentiation ◽  
Epithelial Cells ◽  
Stearic Acid ◽  
Er Stress ◽  
Intestinal Epithelial Cells ◽  
Dependent Manner ◽  
Intestinal Epithelial ◽  
High Concentrations ◽  
Induced Apoptosis ◽  
Dose Dependent

Background: Stearic acid (SA), a saturated long-chain fatty acid consisting of 18 carbon atoms, is widely found in feed ingredients, such as corn, soybeans, and wheat. However, the roles of SA in the renewal of intestinal epithelial cells remain unclear. Methods and Results: In the present study, we found that 0.01-0.1 mM SA promoted IPEC-J2 cell differentiation and did not affect IPEC-J2 cell viability. In addition, the results showed that the viability of IPEC-J2 cells was inhibited by SA in a time- and dose-dependent manner at high concentrations. Flow cytometry and western blot analysis suggested that SA induced apoptosis, autophagy and ER stress in cells. In addition, the amounts of triglyceride were significantly increased upon challenge with SA. Moreover, the decrease in the viability of cells induced by SA could be attenuated by 4-PBA, an inhibitor of ER stress. Conclusion: In summary, SA accelerated IPEC-J2 cell differentiation at 0.01-0.1 mM. Furthermore, SA induced IPEC-J2 cell apoptosis and autophagy by causing ER stress.

Modular effects of estradiol on ethanol-induced apoptosis in human intestinal epithelial cells

2005 ◽  
Vol 40 (3) ◽  
pp. 326-335 ◽  
Author(s):  
Kiyoko Asai ◽  
Wim A. Buurman ◽  
Chris P. M. Reutelingsperger ◽  
Bert Schutte ◽  
Michio Kaminishi
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Human Intestinal Epithelial Cells ◽  
Induced Apoptosis

scholarly journals Wingless homolog Wnt11 suppresses bacterial invasion and inflammation in intestinal epithelial cells

2011 ◽  
Vol 301 (6) ◽  
pp. G992-G1003 ◽  
Author(s):  
Xingyin Liu ◽  
Shaoping Wu ◽  
Yinglin Xia ◽  
Xi Emma Li ◽  
Yuxuan Xia ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Pathogenic Bacteria ◽  
Intestinal Inflammation ◽  
Intestinal Epithelial Cells ◽  
Enteric Bacteria ◽  
Bacterial Invasion ◽  
Intestinal Epithelial ◽  
Induced Apoptosis ◽  
In Cells

Wnt11 plays an essential role in gastrointestinal epithelial proliferation, and previous investigations have focused on development and immune responses. However, the roles of how enteric bacteria regulate Wnt11 and how Wnt11 modulates the host response to pathogenic bacteria remain unexplored. This study investigated the effects of Salmonella infection on Wnt activation in intestinal epithelial cells. We found that Wnt11 mRNA and protein expression were elevated after Salmonella colonization. Wnt11 protein secretion in epithelial cells was also elevated after bacterial infection. Furthermore, we demonstrated that pathogenic Salmonella regulated Wnt11 expression and localization in vivo. We found a decrease in Salmonella invasion in cells with Wnt11 overexpression compared with cells with normal Wnt11 level. IL-8 mRNA in Wnt11-transfected cells was low; however, it was enhanced in cells with a low level of Wnt11 expression. Functionally, Wnt11 overexpression inhibited Salmonella-induced apoptosis. AvrA is a known bacterial effector protein that stabilizes β-catenin, the downstream regulator of Wnt signaling, and inhibits bacterially induced intestinal inflammation. We observed that Wnt11 expression, secretion, and transcriptional activity were regulated by Salmonella AvrA. Overall, Wnt11 is involved in the protection of the host intestinal cells by blocking the invasion of pathogenic bacteria, suppressing inflammation, and inhibiting apoptosis. Wnt11 is a novel and important contributor to intestinal homeostasis and host defense.

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