scholarly journals MicroRNA-7-5p regulates the proliferation and migration of intestinal epithelial cells by targeting trefoil factor 3 via inhibiting the phosphoinositide 3-kinase/Akt signalling pathway

2017 ◽  
Vol 40 (5) ◽  
pp. 1435-1443 ◽  
Author(s):  
Jing Guo ◽  
Lingfen Xu ◽  
Xu Teng ◽  
Mei Sun
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Signalling Pathway ◽  
Intestinal Epithelial ◽  
Trefoil Factor ◽  
Trefoil Factor 3 ◽  
And Migration ◽  
Phosphoinositide 3 Kinase ◽  
Proliferation And Migration

scholarly journals IL-22–induced cell extrusion and IL-18–induced cell death prevent and cure rotavirus infection

2020 ◽  
Vol 5 (52) ◽  
pp. eabd2876
Author(s):  
Zhan Zhang ◽  
Jun Zou ◽  
Zhenda Shi ◽  
Benyue Zhang ◽  
Lucie Etienne-Mesmin ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Viral Infections ◽  
Intestinal Epithelial Cells ◽  
Intestinal Lumen ◽  
Intestinal Epithelial ◽  
And Migration ◽  
Rapid Drop ◽  
Cell Extrusion ◽  
Proliferation And Migration

Bacterial flagellin can elicit production of TLR5-mediated IL-22 and NLRC4-mediated IL-18 cytokines that act in concert to cure and prevent rotavirus (RV) infection. This study investigated the mechanism by which these cytokines act to impede RV. Although IL-18 and IL-22 induce each other’s expression, we found that IL-18 and IL-22 both impeded RV independently of one another and did so by distinct mechanisms that involved activation of their cognate receptors in intestinal epithelial cells (IEC). IL-22 drove IEC proliferation and migration toward villus tips, which resulted in increased extrusion of highly differentiated IEC that serve as the site of RV replication. In contrast, IL-18 induced cell death of RV-infected IEC thus directly interrupting the RV replication cycle, resulting in spewing of incompetent virus into the intestinal lumen and causing a rapid drop in the number of RV-infected IEC. Together, these actions resulted in rapid and complete expulsion of RV, even in hosts with severely compromised immune systems. These results suggest that a cocktail of IL-18 and IL-22 might be a means of treating viral infections that preferentially target short-lived epithelial cells.

scholarly journals TFF3 modulates NF-κB and a novel negative regulatory molecule of NF-κB in intestinal epithelial cells via a mechanism distinct from TNF-α

2005 ◽  
Vol 289 (5) ◽  
pp. C1085-C1093 ◽  
Author(s):  
Ya-Qin Zhu ◽  
Xiao-Di Tan
Keyword(s):  
Tumor Necrosis Factor ◽  
Epithelial Cells ◽  
Tumor Necrosis ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Trefoil Factor ◽  
Trefoil Factor 3 ◽  
Twist Protein ◽  
Factor Α ◽  
Necrosis Factor

Trefoil factor 3 (intestinal trefoil factor) is a cytoprotective factor in the gut. Herein we compared the effect of trefoil factor 3 with tumor necrosis factor-α on 1) activation of NF-κB in intestinal epithelial cells; 2) expression of Twist protein (a molecule essential for downregulation of nuclear factor-κB activity in vivo); and 3) production of interleukin-8. We showed that Twist protein is constitutively expressed in intestinal epithelial cells. Tumor necrosis factor-α induced persistent degradation of Twist protein in intestinal epithelial cells via a signaling pathway linked to proteasome, which was associated with prolonged activation of NF-κB. In contrast to tumor necrosis factor, trefoil factor 3 triggered transient activation of NF-κB and prolonged upregulation of Twist protein in intestinal epithelial cells via an ERK kinase-mediated pathway. Unlike tumor necrosis factor-α, transient activation of NF-κB by trefoil factor 3 is not associated with induction of IL-8 in cells. To examine the role of Twist protein in intestinal epithelial cells, we silenced the Twist expression by siRNA. Our data showed that trefoil factor 3 induced interleukin-8 production after silencing Twist in intestinal epithelial cells. Together, these observations indicated that 1) trefoil factor 3 triggers a diverse signal from tumor necrosis factor-α on the activation of NF-κB and its associated molecules in intestinal epithelial cells; and 2) trefoil factor 3-induced Twist protein plays an important role in the modulation of inflammatory cytokine production in intestinal epithelial cells.

scholarly journals IL-22 induced cell extrusion and IL-18-induced pyroptosis prevent and cure rotavirus infection

2019 ◽  
Author(s):  
Zhan Zhang ◽  
Jun Zou ◽  
Zhenda Shi ◽  
Benyue Zhang ◽  
Lucie Etienne-Mesmin ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Viral Infections ◽  
Intestinal Epithelial Cells ◽  
Intestinal Lumen ◽  
Intestinal Epithelial ◽  
Immune Systems ◽  
And Migration ◽  
Rapid Drop ◽  
Cell Extrusion ◽  
Proliferation And Migration

SummaryAdministration of bacterial flagellin elicits production of TLR5-mediated IL-22 and NLRC4-mediated IL-18 that act in concert to cure and prevent rotavirus (RV) infection. This study investigated the mechanism by which these cytokines act to impede this virus. Although IL-18 and IL-22 induce each other’s expression, we found that IL-18 and IL-22 both impeded RV independently of each other and did so by distinct mechanisms, in both cases via activation of their cognate receptors in intestinal epithelial cells (IEC). IL-22 drove IEC proliferation and migration toward villus tips, which resulted in increased extrusion of highly differentiated IEC that serve as the site of RV replication. In contrast, IL-18 induced pyroptotic death of RV-infected IEC thus directly interrupting the RV replication cycle, resulting in spewing of incompetent virus into the intestinal lumen and causing a rapid drop in levels of RV-infected IEC. Together, these actions resulted in rapid and complete expulsion of RV, even in hosts with severely compromised immune systems. These results suggest that IL-18/22 might be a means of treating viral infections that preferentially target short-lived epithelial cells.

A thermal injury-induced circulating factor(s) compromises intestinal cell morphology, proliferation, and migration

1999 ◽  
Vol 277 (1) ◽  
pp. G175-G182 ◽  
Author(s):  
Maryam Varedi ◽  
George H. Greeley ◽  
David N. Herndon ◽  
Ella W. Englander
Keyword(s):  
Epithelial Cells ◽  
Thermal Injury ◽  
Intestinal Epithelial Cells ◽  
Intestinal Cell ◽  
Intestinal Epithelial ◽  
Rat Serum ◽  
In Vitro Effects ◽  
Mucosal Morphology ◽  
And Migration

The effects of a 60% body surface area thermal injury in rats on the morphology and proliferation of the epithelium of the small intestine and the in vitro effects of serum collected from scalded rats on intestinal epithelial cells were investigated. Scald injury caused significant reductions in duodenal villus width and crypt dimensions, villus enterocytes changed in shape from columnar to cuboidal, and the number of goblet cells decreased. The proportion of bromodeoxyuridine-labeled S phase cells in crypts was also diminished. In vitro, incubation of intestinal epithelial cells (IEC-6) with scalded rat serum (SRS) collected at either 12 or 24 h after injury caused a disruption in the integrity of the confluent culture and induced the appearance of large denuded areas. SRS also decreased DNA synthesis and delayed wound closure in an in vitro wound-healing model. The thermal injury-induced changes in intestinal mucosal morphology and epithelial cell growth characteristics described in this study may underlie, in part, the mechanism(s) involved in the diminished absorption of nutrients, increased intestinal permeability, and sepsis in patients with thermal injury.

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