scholarly journals Expression of fibronectin and tenascin-C mRNA by myofibroblasts, vascular cells and epithelial cells in human colon adenomas and carcinomas

1997 ◽  
Vol 73 (1) ◽  
pp. 10-15 ◽  
Author(s):  
Noriko Hanamura ◽  
Toshimichi Yoshida ◽  
Ei-ichi Matsumoto ◽  
Yoshifumi Kawarada ◽  
Teruyo Sakakura
Keyword(s):  
Epithelial Cells ◽  
Human Colon ◽  
Vascular Cells ◽  
Tenascin C ◽  
Colon Adenomas

Enterocytes are the primary source of the chemokine ENA-78 in normal colon and ulcerative colitis

1997 ◽  
Vol 273 (1) ◽  
pp. G75-G82 ◽  
Author(s):  
S. Keates ◽  
A. C. Keates ◽  
E. Mizoguchi ◽  
A. Bhan ◽  
C. P. Kelly
Keyword(s):  
Ulcerative Colitis ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Primary Source ◽  
Fold Increase ◽  
Human Colon ◽  
Neutrophil Recruitment ◽  
Normal Colon ◽  
Necrosis Factor Alpha ◽  
Cytokine Stimulation

Epithelial cell-derived neutrophil-activating protein-78 (ENA-78) is a neutrophil-directed C-X-C chemokine. We report that Caco-2 and T84 human intestinal epithelial cells produce ENA-78 after stimulation by interleukin (IL)-1 beta or tumor necrosis factor-alpha. Caco-2 cells show increased IL-8 production at 4-12 h and increased ENA-78 production at 8-24 h after cytokine stimulation. Immunohistochemical studies in normal human colon and in ulcerative colitis demonstrate ENA-78 immunoreactivity principally associated with crypt epithelial cells. Furthermore, human colonic tissues from patients with ulcerative colitis show elevated levels of ENA-78 mRNA (24-fold increase, P < 0.01) and protein (4-fold increase, P < 0.05) compared with normal controls. Thus ENA-78 is produced in normal colon and in ulcerative colitis and is predominantly of enterocyte origin. The kinetics of ENA-78 induction in human colon epithelial cell lines are delayed and prolonged compared with IL-8. We propose that ENA-78 and IL-8 serve complementary and sequential roles in neutrophil recruitment in ulcerative colitis. ENA-78 as an enterocyte-derived, neutrophil-activating chemokine may be especially important in neutrophil recruitment from the lamina propria into the epithelial layer.

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 A Micro-engineered Human Colon Intestine-Chip Platform to Study Leaky Barrier

2020 ◽  
Author(s):  
Athanasia Apostolou ◽  
Rohit A. Panchakshari ◽  
Antara Banerjee ◽  
Dimitris V. Manatakis ◽  
Maria D. Paraskevopoulou ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelium ◽  
Unmet Need ◽  
Intestinal Barrier ◽  
Human Colon ◽  
Epithelial Barrier ◽  
Host Immune System ◽  
Intestinal Epithelial ◽  
Barrier Disruption ◽  
Interleukin 22

ABSTRACTThe intestinal epithelial barrier supports the symbiotic relationship between the microbiota colonizing the intestinal epithelium and the host immune system to maintain homeostasis. Leaky barrier is increasingly recognized as part of the pathogenesis of a number of chronic conditions in addition to inflammatory and infectious diseases. As our understanding on the regulation of the barrier remains limited, effective therapeutic targeting for the compromised barrier is still an unmet need. Here we combined advancements on the organoids and Organ-on-Chip technologies to establish a micro-engineered Colon Intestine-Chip for studying development and regulation of the human intestinal barrier. Our data demonstrate the significance of the endothelium in co-culture with the epithelial cells within a tissue-relevant microenvironment for the establishment of a tight epithelial barrier of polarized cells. Pathway analysis of the RNA sequencing (RNA-Seq), revealed significant upregulation of mechanisms relevant to the maturation of the intestinal epithelium in organoid-derived epithelial cells in co-culture with endothelium as compared to organoids maintained in suspension. We provide evidence that the Colon Intestine-Chip platform responds to interferon gamma (IFNγ), a prototype cytokine utilized to model inflammation-induced barrier disruption, by induction of apoptosis and reorganization of the apical junctional complexes as shown with other systems. We also describe the mechanism of action of interleukin 22 (IL-22) on mature, organoid-derived intestinal epithelial cells that is consistent with barrier disruption. Overall we propose the Colon Intestine-Chip as a promising human organoid-derived platform to decipher mechanisms driving the development of leaky gut in patients and enable their translation for this unmet medical need.

scholarly journals Cathelicidin Mediates a Protective Role of Vitamin D in Ulcerative Colitis and Human Colonic Epithelial Cells

2020 ◽  
Vol 26 (6) ◽  
pp. 885-897 ◽  
Author(s):  
John Gubatan ◽  
Gillian A Mehigan ◽  
Fernando Villegas ◽  
Shuji Mitsuhashi ◽  
Maria Serena Longhi ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Ulcerative Colitis ◽  
Vitamin D ◽  
Antimicrobial Activity ◽  
Epithelial Cells ◽  
Human Colon ◽  
Protective Role ◽  
Colonic Epithelial Cells ◽  
Colon Cells ◽  
Dss Colitis

Abstract Background Vitamin D plays a protective role in ulcerative colitis (UC) patients through unclear mechanisms. Cathelicidin is an antimicrobial peptide induced by 1,25(OH)D2. Our goal was to evaluate the link between cathelicidin and vitamin D–associated clinical outcomes in UC patients, explore vitamin D induction of cathelicidin in human colon cells, and evaluate the effects of intrarectal human cathelicidin on a murine model of colitis. Methods Serum and colonic cathelicidin levels were measured in UC patients and correlated with clinical and histologic outcomes. Human colon cells were treated with 1,25(OH)2D and production of cathelicidin and cytokines were quantified. Antimicrobial activity against Escherichia coli from cell culture supernatants was measured. Mice were treated with intrarectal cathelicidin, and its effects on DSS colitis and intestinal microbiota were evaluated. Results In UC patients, serum 25(OH)D positively correlated with serum and colonic cathelicidin. Higher serum cathelicidin is associated with decreased risk of histologic inflammation and clinical relapse but not independent of 25(OH)D or baseline inflammation. The 1,25(OH)2D treatment of colon cells induced cathelicidin and IL-10, repressed TNF-α, and suppressed Escherichia coli growth. This antimicrobial effect was attenuated with siRNA-cathelicidin transfection. Intrarectal cathelicidin reduced the severity of DSS colitis but did not mitigate the impact of colitis on microbial composition. Conclusions Cathelicidin plays a protective role in 25(OH)D-associated UC histologic outcomes and murine colitis. Cathelicidin is induced by vitamin D in human colonic epithelial cells and promotes antimicrobial activity against E. coli. Our study provides insights into the vitamin D–cathelicidin pathway as a potential therapeutic target.

scholarly journals Generation of an inducible colon-specific Cre enzyme mouse line for colon cancer research

2016 ◽  
Vol 113 (42) ◽  
pp. 11859-11864 ◽  
Author(s):  
Paul W. Tetteh ◽  
Kai Kretzschmar ◽  
Harry Begthel ◽  
Maaike van den Born ◽  
Jeroen Korving ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Small Intestine ◽  
Epithelial Cells ◽  
Mouse Model ◽  
Human Colon ◽  
Suppressor Gene ◽  
Proximal Colon ◽  
Tumor Formation ◽  
Cell Of Origin ◽  
Human Colon Cancer

Current mouse models for colorectal cancer often differ significantly from human colon cancer, being largely restricted to the small intestine. Here, we aim to develop a colon-specific inducible mouse model that can faithfully recapitulate human colon cancer initiation and progression. Carbonic anhydrase I (Car1) is a gene expressed uniquely in colonic epithelial cells. We generated a colon-specific inducible Car1CreER knock-in (KI) mouse with broad Cre activity in epithelial cells of the proximal colon and cecum. Deletion of the tumor suppressor gene Apc using the Car1CreER KI caused tumor formation in the cecum but did not yield adenomas in the proximal colon. Mutation of both Apc and Kras yielded microadenomas in both the cecum and the proximal colon, which progressed to macroadenomas with significant morbidity. Aggressive carcinomas with some invasion into lymph nodes developed upon combined induction of oncogenic mutations of Apc, Kras, p53, and Smad4. Importantly, no adenomas were observed in the small intestine. Additionally, we observed tumors from differentiated Car1-expressing cells with Apc/Kras mutations, suggesting that a top-down model of intestinal tumorigenesis can occur with multiple mutations. Our results establish the Car1CreER KI as a valuable mouse model to study colon-specific tumorigenesis and metastasis as well as cancer-cell-of-origin questions.

Regulated expression of Gb3 synthase and the shiga-like toxin (STX) receptor Gb3 in human colon epithelial cells

2001 ◽  
Vol 120 (5) ◽  
pp. A327
Author(s):  
Arlette Darfeuille-Michaud ◽  
Michael P. Housley ◽  
Martin F. Kagnoff
Keyword(s):  
Epithelial Cells ◽  
Human Colon ◽  
Regulated Expression
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