scholarly journals Regulated production of the chemokine CCL28 in human colon epithelium

2004 ◽  
Vol 287 (5) ◽  
pp. G1062-G1069 ◽  
Author(s):  
Hiroyuki Ogawa ◽  
Mitsutoshi Iimura ◽  
Lars Eckmann ◽  
Martin F. Kagnoff
Keyword(s):  
Epithelial Cells ◽  
Mrna Expression ◽  
Proinflammatory Cytokine ◽  
Human Colon ◽  
Epithelial Cell Lines ◽  
Normal Human ◽  
Small Intestinal ◽  
Human Intestinal Epithelium ◽  
Colon Epithelial Cell

The chemokine CCL28 is constitutively expressed by epithelial cells at several mucosal sites and is thought to function as a homeostatic chemoattractant of subpopulations of T cells and IgA B cells and to mediate antimicrobial activity. We report herein on the regulation of CCL28 in human colon epithelium by the proinflammatory cytokine IL-1, bacterial flagellin, and n-butyrate, a product of microbial metabolism. In vivo, CCL28 was markedly increased in the epithelium of pathologically inflamed compared with normal human colon. Human colon and small intestinal xenografts were used to model human intestinal epithelium in vivo. Xenografts constitutively expressed little, if any, CCL28 mRNA or protein. After stimulation with the proinflammatory cytokine IL-1, CCL28 mRNA and protein were significantly increased in the epithelium of colon but not small intestinal xenografts, although both upregulated the expression of another prototypic chemokine, CXCL8, in response to the identical stimulus. In studies of CCL28 regulation using human colon epithelial cell lines, proinflammatory stimuli, including IL-1, bacterial flagellin, and bacterial infection, significantly upregulated CCL28 mRNA expression and protein production. In addition, CCL28 mRNA expression and protein secretion by those cells were significantly increased by the short-chain fatty acid n-butyrate, and IL-1- or flagellin-stimulated upregulation of CCL28 by colon epithelial cells was synergistically increased by pretreatment of cells with n-butyrate. Consistent with its upregulated expression by proinflammatory stimuli, CCL28 mRNA expression was attenuated by pharmacological inhibitors of NF-κB activation. These findings indicate that CCL28 functions as an “inflammatory” chemokine in human colon epithelium and suggest the notion that CCL28 may act to counterregulate colonic inflammation.

Normal human colon epithelial cells propagated in long-term cell cultures support JC polyomavirus infection

2001 ◽  
Vol 33 ◽  
pp. A40
Author(s):  
Farhad F. Shadan ◽  
Luigi Ricciardiello ◽  
Ajay Goel ◽  
Wendy Smith ◽  
Dong K. Chang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cell Cultures ◽  
Human Colon ◽  
Jc Polyomavirus ◽  
Normal Human

scholarly journals Expression of c-myc proto-oncogene in normal human intestinal epithelium.

1989 ◽  
Vol 37 (4) ◽  
pp. 541-545 ◽  
Author(s):  
J ten Kate ◽  
S Eidelman ◽  
F T Bosman ◽  
I Damjanov
Keyword(s):  
In Situ Hybridization ◽  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Human Colon ◽  
Intestinal Epithelial ◽  
Cell Compartments ◽  
Entire Thickness ◽  
Normal Human ◽  
Human Intestinal Epithelium

We studied the expression of the human c-myc proto-oncogene in normal human colon epithelium by both in situ hybridization and immunohistochemistry. c-myc was found to be expressed uniformly throughout the entire thickness of the colon epithelium. The present findings do not support the contention that the c-myc proto-oncogene is primarily expressed in proliferating intestinal epithelial cell compartments.

Differences in TRAIL-induced changes of Mcl-1 expression among distinct human colon epithelial cell lines

2009 ◽  
Vol 315 (19) ◽  
pp. 3259-3266 ◽  
Author(s):  
Alena Vaculová ◽  
Jiřina Hofmanová ◽  
Jiřina Zatloukalová ◽  
Alois Kozubík
Keyword(s):  
Epithelial Cell ◽  
Cell Lines ◽  
Human Colon ◽  
Epithelial Cell Lines ◽  
Induced Changes ◽  
Colon Epithelial Cell

Superoxide production in DLD-1 and HT-29 cell lines and in primary epithelial cells from normal human colon

2000 ◽  
Vol 118 (4) ◽  
pp. A98
Author(s):  
Anders Perner ◽  
Lars Andresen ◽  
Gitte Pedersen ◽  
Torben Saermark ◽  
Jorn Brynskov ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cell Lines ◽  
Human Colon ◽  
Superoxide Production ◽  
Normal Human ◽  
Ht 29

scholarly journals Cell-to-Cell Contact as an Efficient Mode of Epstein-Barr Virus Infection of Diverse Human Epithelial Cells

1998 ◽  
Vol 72 (5) ◽  
pp. 4371-4378 ◽  
Author(s):  
Shosuke Imai ◽  
Jun Nishikawa ◽  
Kenzo Takada
Keyword(s):  
Epithelial Cells ◽  
Cell Lines ◽  
Viral Gene Expression ◽  
Viral Gene ◽  
Cell Contact ◽  
Barr Virus ◽  
Epithelial Cell Lines ◽  
Epstein Barr

ABSTRACT We show clear evidence for direct infection of various human epithelial cells by Epstein-Barr virus (EBV) in vitro. The successful infection was achieved by using recombinant EBV (Akata strain) carrying a selective marker gene but without any other artificial operations, such as introduction of the known EBV receptor (CD21) gene or addition of polymeric immunoglobulin A against viral gp350 in culture. Of 21 human epithelial cell lines examined, 18 became infected by EBV, as ascertained by the detection of EBV-determined nuclear antigen (EBNA) 1 expression in the early period after virus exposure, and the following selection culture easily yielded a number of EBV-infected clones from 15 cell lines. None of the human fibroblasts and five nonhuman-derived cell lines examined was susceptible to the infection. By comparison, cocultivation with virus producers showed ≈800-fold-higher efficiency of infection than cell-free infection did, suggesting the significance of direct cell-to-cell contact as a mode of virus spread in vivo. Most of the epithelial cell lines infectable with EBV were negative for CD21 expression at the protein and mRNA levels. The majority of EBV-infected clones established from each cell line invariably expressed EBNA1, EBV-encoded small RNAs, rightward transcripts from theBamHI-A region of the virus genome, and latent membrane protein (LMP) 2A, but not the other EBNAs or LMP1. This restricted form of latent viral gene expression, which is a central issue for understanding epithelial oncogenesis by EBV, resembled that seen in EBV-associated gastric carcinoma and LMP1-negative nasopharyngeal carcinoma. The results indicate that direct infection of epithelial cells by EBV may occur naturally in vivo, and this could be mediated by an unidentified, epithelium-specific binding receptor for EBV. The EBV convertants are viewed, at least in terms of viral gene expression, as in vitro analogs of EBV-associated epithelial tumor cells, thus facilitating analysis of an oncogenic role(s) for EBV in epithelial cells.

Prolonged interferon-γ exposure decreases ion transport, NKCC1, and Na+-K+-ATPase expression in human intestinal xenografts in vivo

2004 ◽  
Vol 286 (1) ◽  
pp. G157-G165 ◽  
Author(s):  
Lone S. Bertelsen ◽  
Lars Eckmann ◽  
Kim E. Barrett
Keyword(s):  
Ion Transport ◽  
Prolonged Exposure ◽  
Intestinal Inflammation ◽  
Interferon Γ ◽  
Α Subunit ◽  
Ussing Chambers ◽  
Epithelial Cell Lines ◽  
Ifn Γ ◽  
Small Intestinal

IFN-γ is elevated in intestinal inflammation and alters barrier and transport functions in human colonic epithelial cell lines, but its effects on normal human small intestinal epithelium in vivo are poorly defined. We investigated effects of prolonged IFN-γ exposure on ion transport and expression of transporters by using human fetal small intestinal xenografts. Xenograft-bearing mice were injected with IFN-γ, and 24 h later xenografts were harvested and mounted in Ussing chambers. Baseline potential difference (PD) was not affected by IFN-γ treatment. However, conductance was enhanced and agonist-stimulated ion transport was decreased. IFN-γ also decreased expression of the Na+-K+-2Cl- cotransporter and the α-subunit of Na+-K+-ATPase compared with controls, whereas levels of the calcium-activated Cl- channel and CFTR were unaltered. Thus prolonged exposure to IFN-γ leads to decreased ion secretion due, in part, to decreased ion transporter levels. These findings demonstrate the implications of elevated IFN-γ levels in human small intestine and validate the human intestinal xenograft as a model to study chronic effects of physiologically relevant stimuli.

scholarly journals Cell Differentiation Is a Key Determinant of Cathelicidin LL-37/Human Cationic Antimicrobial Protein 18 Expression by Human Colon Epithelium

2002 ◽  
Vol 70 (2) ◽  
pp. 953-063 ◽  
Author(s):  
Koji Hase ◽  
Lars Eckmann ◽  
John D. Leopard ◽  
Nissi Varki ◽  
Martin F. Kagnoff
Keyword(s):  
Cell Differentiation ◽  
Epithelial Cells ◽  
Antimicrobial Peptides ◽  
Expression Patterns ◽  
Human Colon ◽  
Antimicrobial Protein ◽  
Necrosis Factor Alpha ◽  
Innate Defense ◽  
Regulated Expression

ABSTRACT Antimicrobial peptides are highly conserved evolutionarily and are thought to play an important role in innate immunity at intestinal mucosal surfaces. To better understand the role of the antimicrobial peptide human cathelicidin LL-37/human cationic antimicrobial protein 18 (hCAP18) in intestinal mucosal defense, we characterized the regulated expression and production of this peptide by human intestinal epithelium. LL-37/hCAP18 is shown to be expressed within epithelial cells located at the surface and upper crypts of normal human colon. Little or no expression was seen within the deeper colon crypts or within epithelial cells of the small intestine. Paralleling its expression in more differentiated epithelial cells in vivo, LL-37/hCAP18 mRNA and protein expression was upregulated in spontaneously differentiating Caco-2 human colon epithelial cells and in HCA-7 human colon epithelial cells treated with the cell differentiation-inducing agent sodium butyrate. LL-37/hCAP18 expression by colon epithelium does not require commensal bacteria, since LL-37/hCAP18 is produced with a similar expression pattern by epithelial cells in human colon xenografts that lack a luminal microflora. LL-37/hCAP18 mRNA was not upregulated in response to tumor necrosis factor alpha, interleukin 1α (IL-1α), gamma interferon, lipopolysaccharide, or IL-6, nor did the expression patterns and levels of LL-37/hCAP18 in the epithelium of the normal and inflamed colon differ. On the other hand, infection of HCA-7 cells with Salmonella enterica serovar Dublin or enteroinvasive Escherichia coli modestly upregulated LL-37/hCAP18 mRNA expression. We conclude that differentiated human colon epithelium expresses LL-37/hCAP18 as part of its repertoire of innate defense molecules and that the distribution and regulated expression of LL-37/hCAP18 in the colon differs markedly from that of other enteric antimicrobial peptides, such as defensins.

Growth hormone acts on the synthesis and secretion of α-casein in bovine mammary epithelial cells

2005 ◽  
Vol 72 (3) ◽  
pp. 264-270 ◽  
Author(s):  
Kazuhito Sakamoto ◽  
Tokushi Komatsu ◽  
Takuya Kobayashi ◽  
Michael T Rose ◽  
Hisashi Aso ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Epithelial Cells ◽  
Mrna Expression ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Gh Treatment ◽  
Bovine Mammary Epithelial Cells ◽  
Lactogenic Hormone ◽  
Mammary Epithelia

To study the effect of growth hormone (GH) on the functions of mammary epithelia, we examined the effect of GH on the synthesis and secretion of α-casein in a bovine mammary epithelial cell (BMEC) clonal line, which was established from a 26-d-pregnant Holstein heifer. GH receptors (GHR) were observed in the BMEC on the membrane as well as in the cytoplasm. After BMEC were plated onto cell culture inserts, GH stimulated α-casein release in both the presence and absence of the lactogenic hormone complex, which included dexamethasone, insulin and prolactin (DIP). DIP enhanced the effect of GH on α-casein release. Although αs1-casein mRNA expression was not detected in untreated control cells, its expression was observed in BMEC in response to the GH, DIP and GH+DIP treatments. Expression was greater for GH and GH+DIP than for just DIP. Expression of GHR mRNA was increased by DIP treatment, while the mRNA expression was little changed by GH treatment. We conclude that GH acts on BMEC and induces the expression of both the α-casein gene and protein. GHR gene expression was shown to be regulated by DIP and GHR. GHR may be involved in a synergic effect between GH and DIP on casein secretion. These results suggest that GH, in addition to its widely accepted homeorhetic role in vivo, also can act on the mammary parenchyma, and that the effects of GH on mammary epithelial cells could partly account for the clear galactopoietic effect of recombinant bovine GH seen in lactating dairy cows.

Sign in / Sign up

Export Citation Format

Share Document