scholarly journals Functional transcriptomics in diverse intestinal epithelial cell types reveals robust gut microbial sensitivity of microRNAs in intestinal stem cells

2016 ◽  
Author(s):  
Bailey C. E. Peck ◽  
Amanda T. Mah ◽  
Wendy A. Pitman ◽  
Shengli Ding ◽  
P. Kay Lund ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Intestinal Epithelium ◽  
Mirna Expression ◽  
Intestinal Epithelial Cell ◽  
Ex Vivo ◽  
Cell Types ◽  
Gastrointestinal Diseases ◽  
Host Immune System ◽  
Intestinal Epithelial ◽  
Novel Therapeutic Strategies

ABSTRACTGut microbiota play an important role in regulating the development of the host immune system, metabolic rate, and at times, disease pathogenesis. The factors and mechanisms that mediate communication between microbiota and the intestinal epithelium are poorly understood. We provide novel evidence that microbiota may control intestinal epithelial stem cell (IESC) proliferation in part through microRNAs (miRNAs). We demonstrate that miRNA profiles differ dramatically across functionally distinct cell types of the mouse jejunal intestinal epithelium and that miRNAs respond to microbiota in a highly cell-type specific manner. Importantly, we also show that miRNAs in IESCs are more prominently regulated by microbiota compared to miRNAs in any other intestinal epithelial cell (IEC) subtype. We identify miR-375 as one miRNA that is significantly suppressed by the presence of microbiota in IESCs. Using a novel method to knockdown gene and miRNA expression ex vivo enteroids, we demonstrate that we can knockdown gene expression in Lgr5+ IESCs. Furthermore, when we knockdown miR-375 in IESCs, we observe significantly increased proliferative capacity. Understanding the mechanisms by which microbiota regulate miRNA expression in IESCs and other IEC subtypes will elucidate a critical molecular network that controls intestinal homeostasis and, given the heightened interest in miRNA-based therapies, may offer novel therapeutic strategies in the treatment of gastrointestinal diseases associated with altered IESC function.

scholarly journals Differential Alteration in Intestinal Epithelial Cell Expression of Toll-Like Receptor 3 (TLR3) and TLR4 in Inflammatory Bowel Disease

2000 ◽  
Vol 68 (12) ◽  
pp. 7010-7017 ◽  
Author(s):  
Elke Cario ◽  
Daniel K. Podolsky
Keyword(s):  
Inflammatory Bowel Disease ◽  
Epithelial Cell ◽  
Intestinal Epithelium ◽  
Bowel Disease ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Innate Response ◽  
Response System ◽  
Inflammatory Bowel

ABSTRACT Initiation and perpetuation of the inflammatory intestinal responses in inflammatory bowel disease (IBD) may result from an exaggerated host defense reaction of the intestinal epithelium to endogenous lumenal bacterial flora. Intestinal epithelial cell lines constitutively express several functional Toll-like receptors (TLRs) which appear to be key regulators of the innate response system. The aim of this study was to characterize the expression pattern of TLR2, TLR3, TLR4, and TLR5 in primary intestinal epithelial cells from patients with IBD. Small intestinal and colonic biopsy specimens were collected from patients with IBD (Crohn's disease [CD], ulcerative colitis [UC]) and controls. Non-IBD specimens were assessed by immunofluorescence histochemistry using polyclonal antibodies specific for TLR2, TLR3, TLR4, and TLR5. Primary intestinal epithelial cells (IEC) of normal mucosa constitutively expressed TLR3 and TLR5, while TLR2 and TLR4 were only barely detectable. In active IBD, the expression of TLR3 and TLR4 was differentially modulated in the intestinal epithelium. TLR3 was significantly downregulated in IEC in active CD but not in UC. In contrast, TLR4 was strongly upregulated in both UC and CD. TLR2 and TLR5 expression remained unchanged in IBD. These data suggest that IBD may be associated with distinctive changes in selective TLR expression in the intestinal epithelium, implying that alterations in the innate response system may contribute to the pathogenesis of these disorders.

Alarin in different human intestinal epithelial cell types

2019 ◽  
Vol 151 (6) ◽  
pp. 513-520 ◽  
Author(s):  
Samir Jabari ◽  
Falk Schrödl ◽  
Alexandra Kaser-Eichberger ◽  
Barbara Kofler ◽  
Axel Brehmer
Keyword(s):  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Cell Types ◽  
Intestinal Epithelial ◽  
Human Intestinal Epithelial Cell

scholarly journals Gallic acid affects intestinal-epithelial-cell integrity and selected amino-acid uptake in porcine in vitro and ex vivo permeability models

2020 ◽  
pp. 1-9
Author(s):  
Marco Tretola ◽  
Giuseppe Bee ◽  
Paolo Silacci
Keyword(s):  
Amino Acid ◽  
Epithelial Cell ◽  
Protein Expression ◽  
Gallic Acid ◽  
Intestinal Epithelial Cell ◽  
Ex Vivo ◽  
Amino Acid Transporter ◽  
Intestinal Epithelial ◽  
Cell Integrity

Abstract Gallic acid (GA) is widely used as a dietary supplement due to several health-promoting effects, although its effects on intestinal-epithelial-cell integrity and transport remain mostly unknown. The present study aims to clarify the effects of GA on tight junctions and intestinal nutrient uptake through in vitro and ex vivo models. Both intestinal porcine enterocyte cell line-J2 cells and porcine middle-jejunum segments were treated with 5 (T5), 25 (T25) and 50 (T50) µm GA and mounted in Ussing chambers to determine transepithelial resistance (TEER), claudin-1 (CLDN1), occludin (OCLN), zonula occludens-1 (ZO-1) protein (in tissues and cells) and mRNA (in cells) expression. In addition, uptake of l-glutamate (l-Glut), l-arginine (l-Arg), l-lysine (l-Lys) and l-methionine (l-Meth) together with cationic-amino-acid transporter-1 (CAT-1) and excitatory-amino-acid transporter-3 (EAAT3) expression was evaluated. No apoptosis was observed in GA-treated cells, but TEER and CLDN1 protein abundance was lower with T50 compared with untreated cells. l-Arg and l-Lys uptake was greater with T5 than with T25 and T50. Ex vivo, T50 decreased the TEER values and the protein levels of CLDN1, OCLN and ZO-1, whereas T5 and T25 only decreased CLDN1 protein expression compared with untreated tissues. Moreover, T25 increased l-Glut and l-Arg uptake, the latter confirmed by an increased protein expression of CAT-1. GA influences intestinal uptake of the tested cationic amino acids at low concentrations and decreases the intestinal-cell barrier function at high concentrations. Similarities were observed between in vitro and ex vivo, but different treatment times and structures must be considered.

scholarly journals Intestinal epithelial CD98 synthesis specifically modulates expression of colonic microRNAs during colitis

2012 ◽  
Vol 302 (11) ◽  
pp. G1282-G1291 ◽  
Author(s):  
Moiz A. Charania ◽  
Saravanan Ayyadurai ◽  
Sarah A. Ingersoll ◽  
Bo Xiao ◽  
Emilie Viennois ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Mirna Expression ◽  
Target Genes ◽  
Immune Cell ◽  
Intestinal Inflammation ◽  
Intestinal Epithelial Cells ◽  
Cell Types ◽  
Intestinal Epithelial ◽  
Small Noncoding Rnas

The transmembrane glycoprotein CD98 is known to be involved in intestinal inflammation. In the present study, we found that CD98 overexpression in intestinal epithelial cells does not normally affect the expression of colonic (epithelial and immune cell) microRNAs (miRNAs), small noncoding RNAs that posttranscriptionally regulate a wide variety of biological processes. However, upon dextran sulfate sodium (DSS) treatment, the expression of several colonic miRNAs, but not miRNAs from other tissues such as liver and spleen, were differentially regulated in mice overexpressing CD98 in epithelial cells compared with wild-type (WT) animals. For example, the level of colonic miRNA 132 was not affected by DSS treatment in WT animals but was upregulated in mice overexpressing CD98 in intestinal epithelial cells. Other colonic miRNAs, including colonic miRNA 23a and 23b, were downregulated in WT animals after DSS treatment but not in colonic epithelial cell CD98-overexpressing mice. Interestingly, the expression of potential miRNA target genes affected intestinal epithelial cells that overexpress CD98 and cell types that did not overexpress CD98 but were in close proximity to CD98-overexpressing intestinal epithelial cells. Taken together, these observations show that the combination of an inflammatory context and intestinal epithelial cell expression of CD98 affects the regulation of miRNA expression in colonic epithelial and immune cells. This is new evidence that protein expression modulates miRNA expression and suggests the existence of regulatory crosstalk between proteins and miRNAs in diseases such as colitis.

Ca2+-sensing receptors in intestinal epithelium

1997 ◽  
Vol 273 (4) ◽  
pp. C1168-C1175 ◽  
Author(s):  
Lucio Gama ◽  
Lynn M. Baxendale-Cox ◽  
Gerda E. Breitwieser
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Intestinal Epithelium ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial Cells ◽  
Northern Blotting ◽  
Intestinal Epithelial ◽  
Pcr Products ◽  
Intracellular Ca ◽  
Ht 29

Expression of Ca2+-sensing receptors (CaR) was demonstrated in several human intestinal epithelial cell lines (T84, HT-29, and Caco-2) and in rat intestinal epithelium by both reverse transcriptase-polymerase chain reaction (PCR) and Northern blotting of RNA. Restriction patterns of the PCR products were of the sizes predicted by the human and rat sequences. CaR agonists (Ca2+, poly-l-arginine, protamine) mediated an increase in intracellular Ca2+ in HT-29–18-C1 cells (monitored by changes in fura 2 fluorescence), which was dependent on release from thapsigargin-sensitive stores. U-73122, an inhibitor of phosphatidylinositol-phospholipase C, eliminated the CaR agonist-mediated rise in intracellular Ca2+, whereas its inactive analog, U-73343, had no effect. Pertussis toxin pretreatment had no effect on CaR agonist-mediated modulation of intracellular Ca2+. Taken together, these studies demonstrate that CaR are expressed in intestinal epithelial cells and couple to mobilization of intracellular Ca2+. The presence of CaR in intestinal epithelial cells presents a new locus for investigations into the role(s) of extracellular Ca2+ in modulating intestinal epithelial cell differentiation and transepithelial Ca2+ transport.

Transport features and structural optimization of solid lipid nanoparticles crossing the intestinal epithelium

RSC Advances ◽  
2016 ◽  
Vol 6 (74) ◽  
pp. 70433-70445 ◽  
Author(s):  
Guihong Chai ◽  
Yufang Meng ◽  
Shaoqing Chen ◽  
Fuqiang Hu ◽  
Yong Gan ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Structural Optimization ◽  
Intestinal Epithelium ◽  
Solid Lipid Nanoparticles ◽  
Intestinal Epithelial Cell ◽  
Cell Monolayer ◽  
Lipid Nanoparticles ◽  
Intestinal Epithelial ◽  
Solid Lipid

In vitro simulated intestinal epithelial cell monolayer is a novel avenue to screen optimal SLNs formulations.

Inhibition of intestinal epithelial cell renewal and migration induced by starvation

1963 ◽  
Vol 205 (5) ◽  
pp. 868-872 ◽  
Author(s):  
H. Oliver Brown ◽  
Milton L. Levine ◽  
Martin Lipkin
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Intestinal Epithelium ◽  
Intestinal Epithelial Cell ◽  
Morphological Changes ◽  
Extraction Procedure ◽  
Chemical Extraction ◽  
Cell Renewal ◽  
Intestinal Epithelial ◽  
And Migration

Following starvation in mice, the rate of cell renewal of intestinal epithelium was measured. Injection of thymidine-H3 and microautoradiography, and thymidine-C14 and chemical extraction procedure were utilized. Cell renewal was reduced to about one-half the normal rate following extreme starvation. Morphological changes and impaired differentiation of the epithelial cells accompanied this change. The rate of migration of the epithelial cells to the villus tips was also reduced.

scholarly journals Expression of SARS‐CoV‐2 entry factors, electrolyte, and mineral transporters in different mouse intestinal epithelial cell types

2021 ◽  
Vol 9 (21) ◽  
Author(s):  
Sarah C. Pearce ◽  
Panan Suntornsaratoon ◽  
Kunihiro Kishida ◽  
Arwa Al‐Jawadi ◽  
Joshua Guardia ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Cell Types ◽  
Intestinal Epithelial

scholarly journals Opinion: Are Organoids the End of Model Evolution for Studying Host Intestinal Epithelium/Microbe Interactions?

2019 ◽  
Vol 7 (10) ◽  
pp. 406 ◽  
Author(s):  
Michelle M. George ◽  
Mushfiqur Rahman ◽  
Jessica Connors ◽  
Andrew W. Stadnyk
Keyword(s):  
Epithelial Cell ◽  
Cell Biology ◽  
Intestinal Epithelial Cell ◽  
Spatial Organization ◽  
Ex Vivo ◽  
Model Systems ◽  
Apical Surface ◽  
Intestinal Epithelial ◽  
Intestinal Organoids

In the pursuit to understand intestinal epithelial cell biology in health and disease, researchers have established various model systems, from whole animals (typically rodents) with experimentally induced disease to transformed human carcinomas. The obvious limitation to the ex vivo or in vitro cell systems was enriching, maintaining, and expanding differentiated intestinal epithelial cell types. The popular concession was human and rodent transformed cells of mainly undifferentiated cells, with a few select lines differentiating along the path to becoming goblet cells. Paneth cells, in particular, remained unculturable. The breakthrough came in the last decade with the report of conditions to grow mouse intestinal organoids. Organoids are 3-dimensional ex vivo “mini-organs” of the organ from which the stem cells were derived. Intestinal organoids contain fully differentiated epithelial cells in the same spatial organization as in the native epithelium. The cells are suitably polarized and produce and secrete mucus onto the apical surface. This review introduces intestinal organoids and provide some thoughts on strengths and weaknesses in the application of organoids to further advance our understanding of the intestinal epithelial–microbe relationship.

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