scholarly journals Protective role of berberine on ulcerative colitis through modulating enteric glial cells–intestinal epithelial cells–immune cells interactions

2020 ◽  
Vol 10 (3) ◽  
pp. 447-461 ◽  
Author(s):  
Heng Li ◽  
Chen Fan ◽  
Huimin Lu ◽  
Chunlan Feng ◽  
Peilan He ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Epithelial Cells ◽  
Glial Cells ◽  
Immune Cells ◽  
Intestinal Epithelial Cells ◽  
Protective Role ◽  
Intestinal Epithelial ◽  
Enteric Glial Cells

Prevention of Dextran Sulfate Sodium-induced Mouse Colitis by a Fungal Protein Ling Zhi-8 via Promoting the Barrier Function of Intestinal Epithelial Cells

2021 ◽  
Author(s):  
Yu-Huan Chen ◽  
Jenn-Yeu Shin ◽  
Hsiu-Mei Wei ◽  
Chi-Chen Lin ◽  
Linda Chia-Hui Yu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Immune Cells ◽  
Ganoderma Lucidum ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Fungal Protein ◽  
Fungal Immunomodulatory Protein

A fungal immunomodulatory protein Ling Zhi-8 (LZ-8) isolated from Ganoderma lucidum (GL) regulates immune cells and inhibits tumor growth; however, the role of LZ-8 in intestinal epithelial cells (IECs) is...

scholarly journals Enteric glia promote intestinal mucosal healing via activation of focal adhesion kinase and release of proEGF

2011 ◽  
Vol 300 (6) ◽  
pp. G976-G987 ◽  
Author(s):  
Laurianne Van Landeghem ◽  
Julien Chevalier ◽  
Maxime M. Mahé ◽  
Thilo Wedel ◽  
Petri Urvil ◽  
...  
Keyword(s):  
Wound Healing ◽  
Epithelial Cells ◽  
Glial Cells ◽  
Focal Adhesion ◽  
Intestinal Epithelial Cells ◽  
Mucosal Damage ◽  
Mucosal Healing ◽  
Intestinal Epithelial ◽  
Enteric Glia ◽  
Enteric Glial Cells

Wound healing of the gastrointestinal mucosa is essential for the maintenance of gut homeostasis and integrity. Enteric glial cells play a major role in regulating intestinal barrier function, but their role in mucosal barrier repair remains unknown. The impact of conditional ablation of enteric glia on dextran sodium sulfate (DSS)-induced mucosal damage and on healing of diclofenac-induced mucosal ulcerations was evaluated in vivo in GFAP-HSVtk transgenic mice. A mechanically induced model of intestinal wound healing was developed to study glial-induced epithelial restitution. Glial-epithelial signaling mechanisms were analyzed by using pharmacological inhibitors, neutralizing antibodies, and genetically engineered intestinal epithelial cells. Enteric glial cells were shown to be abundant in the gut mucosa, where they associate closely with intestinal epithelial cells as a distinct cell population from myofibroblasts. Conditional ablation of enteric glia worsened mucosal damage after DSS treatment and significantly delayed mucosal wound healing following diclofenac-induced small intestinal enteropathy in transgenic mice. Enteric glial cells enhanced epithelial restitution and cell spreading in vitro. These enhanced repair processes were reproduced by use of glial-conditioned media, and soluble proEGF was identified as a secreted glial mediator leading to consecutive activation of epidermal growth factor receptor and focal adhesion kinase signaling pathways in intestinal epithelial cells. Our study shows that enteric glia represent a functionally important cellular component of the intestinal epithelial barrier microenvironment and that the disruption of this cellular network attenuates the mucosal healing process.

Characterization of human, mouse, and rat cultures of enteric glial cells and their effect on intestinal epithelial cells

2013 ◽  
Vol 25 (11) ◽  
pp. e755-e764 ◽  
Author(s):  
R. Soret ◽  
S. Coquenlorge ◽  
F. Cossais ◽  
G. Meurette ◽  
M. Rolli-Derkinderen ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Glial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Enteric Glial Cells

scholarly journals Regulation of intestinal epithelial cells transcriptome by enteric glial cells: impact on intestinal epithelial barrier functions

BMC Genomics ◽  
2009 ◽  
Vol 10 (1) ◽  
pp. 507 ◽  
Author(s):  
Laurianne Van Landeghem ◽  
Maxime M Mahé ◽  
Raluca Teusan ◽  
Jean Léger ◽  
Isabelle Guisle ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Glial Cells ◽  
Intestinal Epithelial Cells ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Barrier Functions ◽  
Enteric Glial Cells

scholarly journals Glucocorticoids Promote the Onset of Acute Experimental Colitis and Cancer by Upregulating mTOR Signaling in Intestinal Epithelial Cells

Cancers ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 945 ◽  
Author(s):  
Zhengguo Zhang ◽  
Lin Dong ◽  
Anna Jia ◽  
Xi Chen ◽  
Qiuli Yang ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Epithelial Cells ◽  
Immune Cells ◽  
Cytokine Production ◽  
Immune Cell ◽  
Intestinal Epithelial Cells ◽  
Critical Role ◽  
Mtor Signaling ◽  
Therapeutic Effects ◽  
Intestinal Epithelial

The therapeutic effects of glucocorticoids on colitis and colitis-associated cancer are unclear. In this study, we investigated the therapeutic roles of glucocorticoids in acute experimental ulcerative colitis and colitis-associated cancer in mice and their immunoregulatory mechanisms. Murine acute ulcerative colitis was induced by dextran sulfate sodium (DSS) and treated with dexamethasone (Dex) at different doses. Dex significantly exacerbated the onset and severity of DSS-induced colitis and potentiated mucosal inflammatory macrophage and neutrophil infiltration, as well as cytokine production. Furthermore, under inflammatory conditions, the expression of the glucocorticoid receptor (GR) did not change significantly, while mammalian target of rapamycin (mTOR) signaling was higher in colonic epithelial cells than in colonic immune cells. The deletion of mTOR in intestinal epithelial cells, but not that in myeloid immune cells, in mice significantly ameliorated the severe course of colitis caused by Dex, including weight loss, clinical score, colon length, pathological damage, inflammatory cell infiltration and pro-inflammatory cytokine production. These data suggest that mTOR signaling in intestinal epithelial cells, mainly mTORC1, plays a critical role in the Dex-induced exacerbation of acute colitis and colitis-associated cancer. Thus, these pieces of evidence indicate that glucocorticoid-induced mTOR signaling in epithelial cells is required in the early stages of acute ulcerative colitis by modulating the dynamics of innate immune cell recruitment and activation.

scholarly journals Rspo3 regulates the abnormal differentiation of small intestinal epithelial cells in diabetic state

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Ti-Dong Shan ◽  
Han Yue ◽  
Xue-Guo Sun ◽  
Yue-Ping Jiang ◽  
Li Chen
Keyword(s):  
Epithelial Cells ◽  
Bioinformatics Analysis ◽  
Intestinal Epithelial Cells ◽  
Underlying Mechanism ◽  
Luciferase Reporter ◽  
Intestinal Epithelial ◽  
Epithelial Stem Cells ◽  
Diabetic State ◽  
Definitive Evidence

Abstract Background The complications caused by diabetes mellitus (DM) are the focus of clinical treatment. However, little is known about diabetic enteropathy (DE) and its potential underlying mechanism. Methods Intestinal epithelial cells (IECs) and intestinal epithelial stem cells (IESCs) were harvested from BKS.Cg-Dock7m+/+Leprdb/JNju (DM) mice, and the expression of R-Spondin 3 (Rspo3) was detected by RT-qPCR, Western blotting, immunohistochemistry, and immunofluorescence. The role of Rspo3 in the abnormal differentiation of IECs during DM was confirmed by knockdown experiments. Through miRNA expression profiling, bioinformatics analysis, and RT-qPCR, we further analyzed the differentiation-related miRNAs in the IECs from mice with DM. Results Abnormal differentiation of IECs was observed in the mice with DM. The expression of Rspo3 was upregulated in the IECs from the mice with DM. This phenomenon was associated with Rspo3 overexpression. Additionally, Rspo3 is a major determinant of Lgr5+ stem cell identity in the diabetic state. Microarray analysis, bioinformatics analysis, and luciferase reporter assays revealed that microRNA (miR)-380-5p directly targeted Rspo3. Moreover, miR-380-5p upregulation was observed to attenuate the abnormal differentiation of IECs by regulating Rspo3 expression. Conclusions Together, our results provide definitive evidence of the essential role of Rspo3 in the differentiation of IECs in DM.

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