scholarly journals Association of Protease Activity in Vibrio choleraeVaccine Strains with Decreases in Transcellular Epithelial Resistance of Polarized T84 Intestinal Epithelial Cells

2000 ◽  
Vol 68 (11) ◽  
pp. 6487-6492 ◽  
Author(s):  
Stephanie F. Mel ◽  
Karla Jean Fullner ◽  
Susan Wimer-Mackin ◽  
Wayne I. Lencer ◽  
John J. Mekalanos

ABSTRACT Culture supernatants prepared from reactogenic strains ofVibrio cholerae cause a decrease in the transcellular epithelial resistance of T84 intestinal cells. This decrease correlates with the presence of hemagglutinin/protease but not with the presence of other potential accessory toxins or proteases. These data suggest a possible role for hemagglutinin/protease in reactogenicity, although other factors may also contribute.

2016 ◽  
Vol 7 (10) ◽  
pp. 4388-4399 ◽  
Author(s):  
Anouk Kaulmann ◽  
Sébastien Planchon ◽  
Jenny Renaut ◽  
Yves-Jacques Schneider ◽  
Lucien Hoffmann ◽  
...  

Proteomic response of intestinal cells as a model of inflammatory bowel diseases to digested plum and cabbage rich in polyphenols and carotenoids.


2014 ◽  
Vol 25 (20) ◽  
pp. 3095-3104 ◽  
Author(s):  
Keiko Saegusa ◽  
Miyuki Sato ◽  
Katsuya Sato ◽  
Junko Nakajima-Shimada ◽  
Akihiro Harada ◽  
...  

Intestinal epithelial cells have unique apical membrane structures, known as microvilli, that contain bundles of actin microfilaments. In this study, we report that Caenorhabditis elegans cytosolic chaperonin containing TCP-1 (CCT) is essential for proper formation of microvilli in intestinal cells. In intestinal cells of cct-5(RNAi) animals, a substantial amount of actin is lost from the apical area, forming large aggregates in the cytoplasm, and the apical membrane is deformed into abnormal, bubble-like structures. The length of the intestinal microvilli is decreased in these animals. However, the overall actin protein levels remain relatively unchanged when CCT is depleted. We also found that CCT depletion causes a reduction in the tubulin levels and disorganization of the microtubule network. In contrast, the stability and localization of intermediate filament protein IFB-2, which forms a dense filamentous network underneath the apical surface, appears to be superficially normal in CCT-deficient cells, suggesting substrate specificity of CCT in the folding of filamentous cytoskeletons in vivo. Our findings demonstrate physiological functions of CCT in epithelial cell morphogenesis using whole animals.


PLoS ONE ◽  
2009 ◽  
Vol 4 (11) ◽  
pp. e7806 ◽  
Author(s):  
Gangwei Ou ◽  
Pramod Kumar Rompikuntal ◽  
Aziz Bitar ◽  
Barbro Lindmark ◽  
Karolis Vaitkevicius ◽  
...  

2018 ◽  
Vol 48 (6) ◽  
pp. 2441-2455 ◽  
Author(s):  
Qian Jiang ◽  
Gang Liu ◽  
Jiashun Chen ◽  
Kang Yao ◽  
Yulong Yin

Background/Aims: Lipopolysaccharides (LPSs) act as virulence factors that trigger intestinal inflammation and thereby compromise the production of pigs worldwide. Intestinal diseases and dysfunction have been attributed to endoplasmic reticulum stress (ERS) and the subsequent apoptosis of intestinal epithelial cells. Therefore It is important to explore whether LPSs aggravate ERS-mediated apoptosis of intestinal epithelial cells. Methods: ERS and inflammation models were established in porcine cell line J2 (IPEC-J2) and the cells were treated with tunicamycin or LPS at specific times. The expression of marker proteins was determined by western blot and immunofluorescence. Possible crosstalk between proteins was analyzed by co-immunoprecipitation. Small interfering RNA transfection was employed to verify the mechanisms. Results: We found that Escherichia coli-derived LPS aggravated ERS and ERS-mediated apoptosis in ERS-responsive IPEC-J2 cells. The crosstalk between nuclear glucose-regulated protein 78 (GRP78) and tumor protein 53 (p53) was verified to trigger this LPS-aggravated apoptosis of ERS-responsive intestinal cells. Conclusion: This novel finding implies that intestinal malfunctions might solely originate from the effects of Gram-negative bacteria on ERS-responsive intestinal cells. The regulation of ERS signaling (especially the crosstalk between nuclear GRP78 and p53) in ERS-responsive/rapidly growing intestines may help intestinal cells survive from Gram-negative bacterial infections.


Lab on a Chip ◽  
2018 ◽  
Vol 18 (14) ◽  
pp. 2036-2046 ◽  
Author(s):  
Huanhuan Joyce Chen ◽  
Paula Miller ◽  
Michael L. Shuler

A pumpless GI–Liver system using primary human intestinal epithelial cells serves as an improved model for drug studies.


Sign in / Sign up

Export Citation Format

Share Document