Intestinal epithelial cells express functional interleukin-8-receptors

Sturn, Andreas; Harder-D'heureuse, Johanna; Wiedenmann, B.; Dignaß, Axel

doi:10.1016/s0016-5085(03)82401-0

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“…The intestinal epithelial cells have a critical role in the innate immune response against pathogenic bacteria. In addition to acting as a physical barrier, these cells generate signals by producing several cytokines, chemokines, and other signaling molecules [11][12][13]. In addition, our previous experiment found that the ERS is normally triggered in the rapidly growing intestine, and Escherichia coli infection aggravates CHOP-mediated apoptosis mainly in the jejunal epithelial tissue of weaning stressed piglets [14].…”

Section: Introductionmentioning

confidence: 97%

Crosstalk Between Nuclear Glucose-Regulated Protein 78 and Tumor Protein 53 Contributes to the Lipopolysaccharide Aggravated Apoptosis of Endoplasmic Reticulum Stress-Responsive Porcine Intestinal Epithelial Cells

Jiang¹,

Liu²,

Chen³

et al. 2018

Cell Physiol Biochem

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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.

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