Picotamide inhibition of excess in vitro thromboxane B2 release by colorectal mucosa in inflammatory bowel disease.

1996 ◽  
Vol 10 (3) ◽  
pp. 315-320 ◽  
Author(s):  
CE Collins ◽  
MJ Benson ◽  
WR Burnham ◽  
DS Rampton
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Thromboxane B2 ◽  
Colorectal Mucosa ◽  
Inflammatory Bowel

P140 3D BIOENGINEERED TISSUE MODEL OF THE LARGE INTESTINE TO STUDY INFLAMMATORY BOWEL DISEASE

2020 ◽  
Vol 26 (Supplement_1) ◽  
pp. S34-S35
Author(s):  
Terrence Roh ◽  
Ying Chen ◽  
Harry Paul ◽  
Chengchen Guo ◽  
David Kaplan
Keyword(s):  
Inflammatory Bowel Disease ◽  
Large Intestine ◽  
Intestinal Epithelium ◽  
Bowel Disease ◽  
Tissue Model ◽  
Inflammatory Bowel ◽  
Silk Scaffold ◽  
Subepithelial Layer ◽  
Migration Of Macrophages

Abstract An in vitro model of intestine epithelium with an immune compartment was bioengineered to mimic immunologic responses seen in inflammatory bowel disease [1]. While aspects of intestinal immunity can be modeled in transwells and 2D culture systems, 3D tissue models improve physiological relevance by providing a 3D substrate which enable migration of macrophages towards the epithelium. An intestinal epithelium comprised of non-transformed human colon organoid cells and a subepithelial layer laden with monocyte-derived macrophages was bioengineered to mimic native intestinal mucosa cell organization using spongy silk scaffolds. Confluent epithelial monolayers with microvilli, a mucus layer, and infiltration of macrophages to the basal side of the epithelium were observed. Inflammation, induced by E. coli O111:B4 lipopolysaccharide and interferon γ resulted in morphology changes to the epithelium, resulting in ball-like structures, decreased epithelial coverage, and migration of macrophages to the epithelium. Analysis of cytokines present in the inflamed tissue model demonstrated significantly upregulated secretion of pro-inflammatory cytokines associated with active inflammatory bowel disease, including CXCL10, IL-1β, IL-6, MCP-2, and MIP-1β. The macrophage layer enhanced epithelial and biochemical responses to inflammatory stimuli, and this new tissue system may be useful to study and develop potential therapies for inflammatory bowel disease. References: 6 Roh, T.T., et al., 3D bioengineered tissue model of the large intestine to study inflammatory bowel disease. Biomaterials, 2019: p. 119517. 7 In, J., et al., Enterohemorrhagic Escherichia coli reduce mucus and intermicrovillar bridges in human stem cell-derived colonoids. Cellular and molecular gastroenterology and hepatology, 2015. 2(1): p. 48–62.e3. 8 Chen, Y., et al., In vitro enteroid-derived three-dimensional tissue model of human small intestinal epithelium with innate immune responses. PLoS ONE, 2017. 12(11): p. e0187880. Colonoid and macrophage cultivation scheme in the 3D bilayer system. (A) Human monocytes were isolated from whole blood and human colonoids from large intestine biopsies were cultured according to established protocols [2]. (B) Cell suspensions of colonoids were seeded on the film surface on the inner silk scaffold and monocyte-derived macrophages were seeded throughout the porous outer silk scaffold using established protocols [3]. (C) The model is cultured for 3 weeks total with 2 weeks in High WNT media and 1 week in differentiation media based on established protocol. Colonoids are present in the model throughout the 3 week culture time. 2 sets of macrophages are added with the first set added after the first week of culture and the second set replacing the first set after the second week.

scholarly journals Food and Food Groups in Inflammatory Bowel Disease (IBD): The Design of the Groningen Anti-Inflammatory Diet (GrAID)

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1067
Author(s):  
Marjo J. E. Campmans-Kuijpers ◽  
Gerard Dijkstra
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Food Group ◽  
Dietary Guidelines ◽  
Current Evidence ◽  
Group Level ◽  
Food Groups ◽  
Inflammatory Bowel ◽  
Anti Inflammatory

Diet plays a pivotal role in the onset and course of inflammatory bowel disease (IBD). Patients are keen to know what to eat to reduce symptoms and flares, but dietary guidelines are lacking. To advice patients, an overview of the current evidence on food (group) level is needed. This narrative review studies the effects of food (groups) on the onset and course of IBD and if not available the effects in healthy subjects or animal and in vitro IBD models. Based on this evidence the Groningen anti-inflammatory diet (GrAID) was designed and compared on food (group) level to other existing IBD diets. Although on several foods conflicting results were found, this review provides patients a good overview. Based on this evidence, the GrAID consists of lean meat, eggs, fish, plain dairy (such as milk, yoghurt, kefir and hard cheeses), fruit, vegetables, legumes, wheat, coffee, tea and honey. Red meat, other dairy products and sugar should be limited. Canned and processed foods, alcohol and sweetened beverages should be avoided. This comprehensive review focuses on anti-inflammatory properties of foods providing IBD patients with the best evidence on which foods they should eat or avoid to reduce flares. This was used to design the GrAID.

scholarly journals DNA damage and apoptosis in blood neutrophils of inflammatory bowel disease patients and in Caco-2 cells in vitro exposed to betanin

2016 ◽  
Vol 70 ◽  
pp. 265-271 ◽  
Author(s):  
Małgorzata Zielińska-Przyjemska ◽  
Anna Olejnik ◽  
Agnieszka Dobrowolska-Zachwieja ◽  
Michał Łuczak ◽  
Wanda Baer-Dubowska
Keyword(s):  
Inflammatory Bowel Disease ◽  
Dna Damage ◽  
Bowel Disease ◽  
Blood Neutrophils ◽  
Inflammatory Bowel

scholarly journals Deficiency in the anti-apoptotic protein DJ-1 promotes intestinal epithelial cell apoptosis and aggravates inflammatory bowel disease via p53

2020 ◽  
Vol 295 (13) ◽  
pp. 4237-4251 ◽  
Author(s):  
Jie Zhang ◽  
Min Xu ◽  
Weihua Zhou ◽  
Dejian Li ◽  
Hong Zhang ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Epithelial Cell ◽  
Bowel Disease ◽  
Intestinal Epithelial Cell ◽  
Intestinal Inflammation ◽  
Intestinal Epithelial ◽  
P53 Expression ◽  
Inflammatory Bowel

Parkinson disease autosomal recessive, early onset 7 (PARK7 or DJ-1) is involved in multiple physiological processes and exerts anti-apoptotic effects on multiple cell types. Increased intestinal epithelial cell (IEC) apoptosis and excessive activation of the p53 signaling pathway is a hallmark of inflammatory bowel disease (IBD), which includes ulcerative colitis (UC) and Crohn's disease (CD). However, whether DJ-1 plays a role in colitis is unclear. To determine whether DJ-1 deficiency is involved in the p53 activation that results in IEC apoptosis in colitis, here we performed immunostaining, real-time PCR, and immunoblotting analyses to assess DJ-1 expression in human UC and CD samples. In the inflamed intestines of individuals with IBD, DJ-1 expression was decreased and negatively correlated with p53 expression. DJ-1 deficiency significantly aggravated colitis, evidenced by increased intestinal inflammation and exacerbated IEC apoptosis. Moreover, DJ-1 directly interacted with p53, and reduced DJ-1 levels increased p53 levels both in vivo and in vitro and were associated with decreased p53 degradation via the lysosomal pathway. We also induced experimental colitis with dextran sulfate sodium in mice and found that compared with DJ-1−/− mice, DJ-1−/−p53−/− mice have reduced apoptosis and inflammation and increased epithelial barrier integrity. Furthermore, pharmacological inhibition of p53 relieved inflammation in the DJ-1−/− mice. In conclusion, reduced DJ-1 expression promotes inflammation and IEC apoptosis via p53 in colitis, suggesting that the modulation of DJ-1 expression may be a potential therapeutic strategy for managing colitis.

scholarly journals DOP53 PTPN2 and TiO2 in the pathogenesis of inflammatory bowel disease

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S092-S092
Author(s):  
J Conde ◽  
M Schwarzfischer ◽  
E Katkeviciute ◽  
J Häfliger ◽  
A Niechcial ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Flow Cytometry ◽  
Titanium Dioxide ◽  
Bowel Disease ◽  
Myeloid Cells ◽  
Food Additive ◽  
Inflammasome Activation ◽  
Inflammatory Bowel ◽  
Anti Inflammatory

Abstract Background Inflammatory bowel disease (IBD) is caused by a complex interaction among genetic, immunological, bacterial and environmental factors. In this scenario, protein tyrosine phosphatase non-receptor type-2 (PTPN2) has been recognised as a risk factor for the development of IBD and functional studies revealed a major role for this protein in the development of experimental colitis through the regulation of the inflammasome, among other processes. In the same way, a potential relationship between diet components and IBD was suggested. In fact, it was reported that the food additive titanium dioxide (TiO2) was able to induce inflammasome activation in vitro and increase colitis severity in vivo. These observations led us to hypothesise a putative relationship between PTPN2 and TiO2 that could explain the effects of this microparticle in the pathogenesis of bowel inflammation. Methods DSS colitis model was performed in mice lacking PTPN2 in myeloid cells and their wild-type littermates, treated or not with titanium dioxide. After that, histology studies, flow cytometry, expression analysis, ELISA and barrier function experiments were performed. Also, bone marrow-derived macrophages (BMDMs) were used for in vitro studies. Results Titanium dioxide was able to exacerbate DSS-induced colitis, especially in mice lacking PTPN2 in myeloid cells. Flow cytometry analysis of the lamina propria revealed significant changes in different immune cell populations such as macrophages. In vitro experiments using BMDMs revealed that TiO2 induced the activation of the inflammasome. Also, this microparticle down-regulated the expression of the anti-inflammatory cytokine IL-10 and these effects were mainly mediated by JNK and ERK kinases. Conclusions The food additive titanium dioxide seems to play a negative role in colitis development by affecting the production of pro- and anti-inflammatory mediators in macrophages. This study reveals a new mechanism by which a certain component of the diet modulates intestinal inflammation.

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