scholarly journals Intestinal Protease-Activated Receptor-2 and Fecal Serine Protease Activity are Increased in Canine Inflammatory Bowel Disease and May Contribute to Intestinal Cytokine Expression

2014 ◽  
Vol 76 (8) ◽  
pp. 1119-1127 ◽  
Author(s):  
Shingo MAEDA ◽  
Koichi OHNO ◽  
Kazuyuki UCHIDA ◽  
Hirotaka IGARASHI ◽  
Yuko GOTO-KOSHINO ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Serine Protease ◽  
Bowel Disease ◽  
Protease Activity ◽  
Cytokine Expression ◽  
Serine Protease Activity ◽  
Inflammatory Bowel ◽  
Protease Activated Receptor 2

Mucosal cytokine expression, cellular markers and adhesion molecules in inflammatory bowel disease

1999 ◽  
Vol 11 (3) ◽  
pp. 267-276 ◽  
Author(s):  
Alexander Woywodt ◽  
Diether Ludwig ◽  
Petra Neustock ◽  
Andrea Kruse ◽  
Karsten Schwarting ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Adhesion Molecules ◽  
Bowel Disease ◽  
Cytokine Expression ◽  
Inflammatory Bowel ◽  
Cellular Markers

Tu1885 Pregnane X Receptor Stimulation Reduces NF-κB Mediated Cytokine Expression in Intestinal Biopsies From Inflammatory Bowel Disease Patients

2012 ◽  
Vol 142 (5) ◽  
pp. S-869
Author(s):  
J. Jasper Deuring ◽  
Timon Q. van den Berg ◽  
Ernst J. Kuipers ◽  
Maikel P. Peppelenbosch ◽  
Colin de Haar ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Pregnane X Receptor ◽  
Cytokine Expression ◽  
Receptor Stimulation ◽  
Inflammatory Bowel

Su1306 Protease Activity Analysis and Pathologic Examination on the Same Endoscopic Biopsy Specimen in Inflammatory Bowel Disease

2014 ◽  
Vol 146 (5) ◽  
pp. S-432
Author(s):  
William W. Bivin ◽  
Kofi Clarke ◽  
Crystal Falco ◽  
Sydney D. Finkelstein ◽  
Jan F. Silverman
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Protease Activity ◽  
Biopsy Specimen ◽  
Activity Analysis ◽  
Endoscopic Biopsy ◽  
Pathologic Examination ◽  
Inflammatory Bowel

scholarly journals A Low Dose of Fermented Soy Germ Alleviates Gut Barrier Injury, Hyperalgesia and Faecal Protease Activity in a Rat Model of Inflammatory Bowel Disease

PLoS ONE ◽  
2012 ◽  
Vol 7 (11) ◽  
pp. e49547 ◽  
Author(s):  
Lara Moussa ◽  
Valérie Bézirard ◽  
Christel Salvador-Cartier ◽  
Valérie Bacquié ◽  
Corinne Lencina ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Rat Model ◽  
Bowel Disease ◽  
Protease Activity ◽  
Low Dose ◽  
Gut Barrier ◽  
Inflammatory Bowel

scholarly journals A202 DYSREGULATED ENDOPLASMIC RETICULUM STRESS PATHWAYS IN COLON-DERIVED ENTEROIDS FROM INFLAMMATORY BOWEL DISEASE PATIENTS DRIVE DC MATURATION LEADING TO A PRO-INFLAMMATORY PHENOTYPE

2020 ◽  
Vol 3 (Supplement_1) ◽  
pp. 75-76
Author(s):  
W D Rees ◽  
M Stahl ◽  
K Jacobson ◽  
B Bressler ◽  
L M Sly ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Bowel Disease ◽  
Cytokine Expression ◽  
Stress Markers ◽  
Cytokine Analysis ◽  
Inflammatory Bowel ◽  
Stress Pathway ◽  
Dc Maturation

Abstract Background Intestinal epithelial cells (IECs) rely on danger signals such as adenosine triphosphate (ATP) and endoplasmic reticulum (ER) stress to form an appropriate, coordinated immune response. Moreover, ER stress in IECs contributes to the pathogenesis of inflammatory bowel disease (IBD), and an increase in extracellular ATP concentrations is a risk factor for Crohn’s disease (CD). Aims We hypothesized that cells exposed to ER stress or ATP modulate innate immune responses, creating a pro-inflammatory environment that drives dendritic cell (DC) maturation. Methods Caco-2 cells and human colon-derived enteroid monolayers were exposed to ATP or the ER stress inducer thapsigargin, stimulated with E. coli FliC flagellin, and ER stress markers CHOP, GRP78, and XBP1 s/u were measured via qPCR and western blot, and cytokine release was measured by ELISA. Next, monocyte-derived dendritic cells (moDCs) were cultured in Caco-2 or enteroid conditioned supernatants and their activation status measured via flow cytometry, and cytokine analysis was performed using Luminex platform. We also assessed ER stress markers, TLR5 expression, and cytokine expression differences between IBD and healthy controls (HC). Results We found that ER stress amplified FliC-induced IL-8 and decreased CCL20 in Caco-2 cells. Moreover, in IBD subjects, we found an increase FliC-induced IL-8 response, and decreased TNFa and CCL20. moDCs cultured with conditioned media from Caco-2 or enteroid monolayers showed a proinflammatroy phenotype, with an increase in CD80, CD86, MHCII, and a decrease in CD103. Moreover, moDCs cultured in stressed Caco-2 supernatants increased release of IL-6, TNFa, and IL-12p70, and decreased IL-10, suggesting potential to induce inflammatory Th1 and/or Th17 cells.. DC activation correlated with the amount of FliC-induced IL-8. Interestingly, there were distinct differences in cytokine expression and basal ER stress between IBD and HC enteroid monolayers, suggesting a dysregulated ER stress pathway in IBD-derived enteroids. Conclusions ER stress in Caco-2 cells and colon-derived enteroid monolayers enhances FliC-induced TLR5 responses, leading to a pro-inflammatory environment that drives DC maturation, which may link epithelial ER stress and immune cell activation in IBD. Furthermore, the cytokine and ER stress pathway differences between IBD and HC-derived enteroids suggests that prolonged periods of stress in IBD patients may rewire the IEC stem cell compartment, further perpetuating inflammation and disease. Funding Agencies CCC, CIHR

Cytokine expression in gingival and intestinal tissues of patients with periodontitis and inflammatory bowel disease: An exploratory study

2016 ◽  
Vol 66 ◽  
pp. 141-146 ◽  
Author(s):  
Juliana Santos Bittencourt Menegat ◽  
Ronaldo Lira-Junior ◽  
Mariana Alves Siqueira ◽  
Fernanda Brito ◽  
Ana Teresa Carvalho ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Exploratory Study ◽  
Cytokine Expression ◽  
Inflammatory Bowel

Disease severity predicts bone loss: A longitudinal study in inflammatory bowel disease patients

2001 ◽  
Vol 120 (5) ◽  
pp. A628-A628
Author(s):  
S HENDERSON ◽  
S DHALIWAL ◽  
N HOFFMAN ◽  
R PRINCE
Keyword(s):  
Inflammatory Bowel Disease ◽  
Longitudinal Study ◽  
Bone Loss ◽  
Disease Severity ◽  
Bowel Disease ◽  
Inflammatory Bowel
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