Proteomic response of inflammatory stimulated intestinal epithelial cells to in vitro digested plums and cabbages rich in carotenoids and polyphenols

2016 ◽  
Vol 7 (10) ◽  
pp. 4388-4399 ◽  
Author(s):  
Anouk Kaulmann ◽  
Sébastien Planchon ◽  
Jenny Renaut ◽  
Yves-Jacques Schneider ◽  
Lucien Hoffmann ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Bowel Diseases ◽  
Intestinal Epithelial Cells ◽  
Intestinal Cells ◽  
Intestinal Epithelial ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Proteomic Response

Proteomic response of intestinal cells as a model of inflammatory bowel diseases to digested plum and cabbage rich in polyphenols and carotenoids.

scholarly journals Contribution of Zinc and Zinc Transporters in the Pathogenesis of Inflammatory Bowel Diseases

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Wakana Ohashi ◽  
Toshiyuki Fukada
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Bowel Diseases ◽  
Barrier Function ◽  
Intestinal Epithelial Cells ◽  
Gastrointestinal Diseases ◽  
Zinc Transporters ◽  
Intestinal Epithelial ◽  
Self Renewal ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Intestinal epithelial cells cover the surface of the intestinal tract. The cells are important for preserving the integrity of the mucosal barriers to protect the host from luminal antigens and pathogens. The mucosal barriers are maintained by the continuous and rapid self-renewal of intestinal epithelial cells. Defects in the self-renewal of these cells are associated with gastrointestinal diseases, including inflammatory bowel diseases and diarrhea. Zinc is an essential trace element for living organisms, and zinc deficiency is closely linked to the impaired mucosal integrity. Recent evidence has shown that zinc transporters contribute to the barrier function of intestinal epithelial cells. In this review, we describe the recent advances in understanding the role of zinc and zinc transporters in the barrier function and homeostasis of intestinal epithelial cells.

Signaling pathway via TNF-α/NF-κB in intestinal epithelial cells may be directly involved in colitis-associated carcinogenesis

2009 ◽  
Vol 296 (4) ◽  
pp. G850-G859 ◽  
Author(s):  
Michio Onizawa ◽  
Takashi Nagaishi ◽  
Takanori Kanai ◽  
Ken-ichi Nagano ◽  
Shigeru Oshima ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Maintenance Therapy ◽  
Intestinal Epithelial Cells ◽  
Immunoblot Analysis ◽  
Intestinal Epithelial ◽  
Tnf Receptor ◽  
Tnf Α ◽  
Sequential Administration ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Treatment with anti-TNF-α MAb has been accepted as a successful maintenance therapy for patients with inflammatory bowel diseases (IBD). Moreover, it has been recently reported that blockade of TNF receptor (TNFR) 1 signaling in infiltrating hematopoietic cells may prevent the development of colitis-associated cancer (CAC). However, it remains unclear whether the TNF-α signaling in epithelial cells is involved in the development of CAC. To investigate this, we studied the effects of anti-TNF-α MAb in an animal model of CAC by administration of azoxymethane (AOM) followed by sequential dextran sodium sulfate (DSS) ingestion. We observed that the NF-κB pathway is activated in colonic epithelia from DSS-administered mice in association with upregulation of TNFR2 rather than TNFR1. Immunoblot analysis also revealed that the TNFR2 upregulation accompanied by the NF-κB activation is further complicated in CAC tissues induced in AOM/DSS-administered mice compared with the nontumor area. Such NF-κB activity in the epithelial cells is significantly suppressed by the treatment of MP6-XT22, an anti-TNF-α MAb. Despite inability to reduce the severity of colitis, sequential administration of MP6-XT22 reduced the numbers and size of tumors in association with the NF-κB inactivation. Taken together, present studies suggest that the TNFR2 signaling in intestinal epithelial cells may be directly involved in the development of CAC with persistent colitis and imply that the maintenance therapy with anti-TNF-α MAb may prevent the development of CAC in patients with long-standing IBD.

scholarly journals The food additive E171 and titanium dioxide nanoparticles indirectly alter the homeostasis of human intestinal epithelial cells in vitro

2019 ◽  
Vol 6 (5) ◽  
pp. 1549-1561 ◽  
Author(s):  
Marie Dorier ◽  
David Béal ◽  
Céline Tisseyre ◽  
Caroline Marie-Desvergne ◽  
Muriel Dubosson ◽  
...  
Keyword(s):  
Titanium Dioxide ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Titanium Dioxide Nanoparticles ◽  
Food Additive ◽  
Repeated Exposure ◽  
Intestinal Cells ◽  
Intestinal Epithelial ◽  
Human Intestinal Epithelial Cells

Repeated exposure to E171 or TiO2-NPs, in vitro, induce moderate inflammation and mucus secretion in intestinal cells.

scholarly journals A41 LINKING THE APPENDIX MICROBIOME WITH INFLAMMATORY BOWEL DISEASES

2021 ◽  
Vol 4 (Supplement_1) ◽  
pp. 270-271
Author(s):  
N Arjomand Fard ◽  
H Armstrong ◽  
M W Carroll ◽  
H Q Huynh ◽  
E Wine
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Host Cells ◽  
Intestinal Epithelial ◽  
Related Factors ◽  
Shotgun Metagenomics ◽  
Funding Agencies ◽  
Bowel Diseases ◽  
Recent Method ◽  
Inflammatory Bowel

Abstract Background The appendix has been shown to be associated with the pathogenesis and health outcomes in inflammatory bowel diseases (IBD). Specifically, post appendectomy patients are found to be protective for development of ulcerative colitis (UC); however, mechanisms of appendix involvement remain unclear. Aims Our aim is to examine the microbes associated with the appendix of IBD patients by identifying changes in microbe abundance and interactions with the host in patient cecum luminal washes, collected from close to the neck of the appendix during colonoscopy. We hypothesize that microbes originating in the appendix of IBD patients, through interactions with host-cells in a disrupted microenvironment in the appendix, could contribute to the pathogenesis of UC. Methods Shotgun metagenomics was performed on cecum luminal washes of IBD patients and non-IBD controls. Guided by the metagenomic results, we performed gentamicin protection assays to determine virulence of microbes of interest using Caco2 intestinal epithelial cells. Co-culturing them with human host cells in vitro will identify relevant disease-related factors secreted by microbes and/or host cells using disease models and multiomic approaches. Results Shotgun metagenomics results showed that among numerous microbes, several bacterial taxa demonstrated differences in abundance between IBD and non-IBD patients: Flavonifractor, Bacteroide fragilis, and Alistipes represented 8%, 10%, and 21% abundance respectively in non-IBD patients, while in IBD patients they were present below 0.1%. In contrast, Bacteroide vulgatus and Escherichia coli were about 9% and 69% respectively, in IBD patients, whilst they were present at 1.7% and 1.2% in non-IBD patients, respectively. Following our recent method for validating pathobionts (Armstrong, 2019), we used the gentamicin protection assays to assess the ability of these bacteria to invade Caco2 cells, demonstrating a correlation between invasive potential of these microbes and cecal abundance. Mechanistic experiments, aimed at identifying factors impacting invasion, are in progress. Conclusions These results provide preliminary, but promising findings suggesting mechanisms by which microbiota possibly originating in the appendix may show altered virulence, which may be related to changes in the appendix microenvironment in IBD. With plans in place to increase our patient cohort we will validate these findings. Identifying and profiling these microbes in IBD patients can help improve the understanding of mechanisms underlying microenvironment changes within the appendix and the gut, which could shed light on the role of the appendix in IBD pathogenesis and clarify how microbes drive inflammation in IBD. Funding Agencies CIHR

Amplification loop of the inflammatory process is induced by P2X7R activation in intestinal epithelial cells in response to neutrophil transepithelial migration

2010 ◽  
Vol 299 (1) ◽  
pp. G32-G42 ◽  
Author(s):  
Annabelle Cesaro ◽  
Patrick Brest ◽  
Véronique Hofman ◽  
Xavier Hébuterne ◽  
Scott Wildman ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Active Phase ◽  
Apical Surface ◽  
Intestinal Epithelial ◽  
T84 Cells ◽  
Caspase 1 ◽  
Bowel Diseases ◽  
And Function

Inflammatory bowel diseases (IBD) are characterized during their active phase by polymorphonuclear leukocyte (PMNL) transepithelial migration. The efflux of PMNL into the mucosa is associated with the production of proinflammatory cytokines and the release of ATP from damaged and necrotic cells. The expression and function of purinergic P2X7receptor (P2X7R) in intestinal epithelial cells (IEC) and its potential role in the “cross talk” between IEC and PMNL have not been explored. The aims of the present study were 1) to examine P2X7R expression in IEC (T84 cells) and in human intestinal biopsies; 2) to detect any changes in P2X7R expression in T84 cells during PMNL transepithelial migration, and during the active and quiescent phases of IBD; and 3) to test whether P2X7R stimulation in T84 monolayers can induce caspase-1 activation and IL-1β release by IEC. We found that a functional ATP-sensitive P2X7R is constitutively expressed at the apical surface of IEC T84 cells. PMNL transmigration regulates dynamically P2X7R expression and alters its distribution from the apical to basolateral surface of IEC during the early phase of PMNL transepithelial migration in vitro. P2X7R expression was weak in intestinal biopsies obtained during the active phase of IBD. We show that activation of epithelial P2X7R is mandatory for PMNL-induced caspase-1 activation and IL-1β release by IEC. Overall, these changes in P2X7R function may serve to tailor the intensity of the inflammatory response and to prevent IL-1β overproduction and inflammatory disease.

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