scholarly journals What is IBD (Inflammatory Bowel Disease)?

2019 ◽  
Vol 3 (2) ◽  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Small Intestine ◽  
Digestive Tract ◽  
Large Intestine ◽  
Bowel Disease ◽  
Normal Process ◽  
Waste Products ◽  
Intestinal Diseases ◽  
Life Threatening ◽  
Inflammatory Bowel

Inflammatory bowel disease (IBD) represents a group of intestinal diseases that cause prolonged inflammation of the digestive tract. [The digestive tract comprises the mouth, esophagus, stomach, small intestine and large intestine. It’s responsible for breaking down food, extracting the nutrients and removing any unusable material and waste products. Inflammation anywhere along the digestive tract disrupts this normal process. IBD can be very painful and disruptive and in some cases, it may even be life-threatening.]

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 Diversion colitis: a trigger for ulcerative colitis in the in-stream colon?

Gut ◽  
1999 ◽  
Vol 44 (2) ◽  
pp. 279-282 ◽  
Author(s):  
A G Lim ◽  
F L Langmead ◽  
R M Feakins ◽  
D S Rampton
Keyword(s):  
Ulcerative Colitis ◽  
Inflammatory Bowel Disease ◽  
Risk Factor ◽  
Large Intestine ◽  
Bowel Disease ◽  
Rectosigmoid Colon ◽  
Diversion Colitis ◽  
End Colostomy ◽  
Microscopic Features ◽  
Inflammatory Bowel

The aetiology of ulcerative colitis is unknown. Two patients without pre-existing inflammatory bowel disease in whom end colostomy for faecal incontinence was complicated by diversion colitis in the defunctioned rectosigmoid colon, are described. In both instances, colitis with the clinical, colonoscopic, and microscopic features of ulcerative colitis developed about a year later in the previously normal in-stream colon proximal to the colostomy. These cases suggest that diversion colitis may be a risk factor for ulcerative colitis in predisposed individuals and that ulcerative colitis can be triggered by anatomically discontinuous inflammation elsewhere in the large intestine.

Expanding Contributions of Monogenic Very Early Onset Inflammatory Bowel Disease

2021 ◽  
Author(s):  
Jodie Ouahed
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Early Onset ◽  
Current Issue ◽  
Epithelial Barrier ◽  
Mevalonate Kinase Deficiency ◽  
Bowel Diseases ◽  
Life Threatening ◽  
Mucosal Homeostasis ◽  
Inflammatory Bowel

Abstract Currently over 70 genes known to be causative in very early onset inflammatory bowel disease (VEOIBD) have been identified. In the current issue of Inflammatory Bowel Diseases, 2 articles describing monogenetic forms of VEOIBD are highlighted. One describes a patient with life-threatening VEOIBD and a mutation in ITGA6, illustrating the importance of the epithelial barrier in maintaining mucosal homeostasis. The other describes the presentation and management of 10 patients with VEOIBD secondary to damaging mutations in MVK, resulting in mevalonate kinase deficiency. Though most monogenic causes of VEOIBD remain “private,” understanding the different categories of pathways affected in children with VEOIBD is critical and has already resulted in invaluable insight in the management of patients with VEOIBD and may hold strong implications for the care of IBD overall.

scholarly journals Microbiota-nourishing Immunity and Its Relevance for Ulcerative Colitis

2019 ◽  
Vol 25 (5) ◽  
pp. 811-815 ◽  
Author(s):  
Mariana X Byndloss ◽  
Yael Litvak ◽  
Andreas J Bäumler
Keyword(s):  
Ulcerative Colitis ◽  
Inflammatory Bowel Disease ◽  
Immune System ◽  
Environmental Exposure ◽  
Large Intestine ◽  
Bowel Disease ◽  
Human Diseases ◽  
Colonization Resistance ◽  
Inflammatory Bowel ◽  
New Hypothesis

An imbalance in our microbiota may contribute to many human diseases, but the mechanistic underpinnings of dysbiosis remain poorly understood. We argue that dysbiosis is secondary to a defect in microbiota-nourishing immunity, a part of our immune system that balances the microbiota to attain colonization resistance against environmental exposure to microorganisms. We discuss this new hypothesis and its implications for ulcerative colitis, an inflammatory bowel disease of the large intestine.

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

2020 ◽  
Vol 158 (3) ◽  
pp. S55-S56
Author(s):  
Terrence Roh ◽  
Ying Chen ◽  
Harry Paul ◽  
Chengchen Guo ◽  
David Kaplan
Keyword(s):  
Inflammatory Bowel Disease ◽  
Large Intestine ◽  
Bowel Disease ◽  
Tissue Model ◽  
Inflammatory Bowel

scholarly journals Necroptosis in inflammatory bowel disease and other intestinal diseases

2018 ◽  
Vol 6 (14) ◽  
pp. 745-752 ◽  
Author(s):  
Sha Li ◽  
Long-Gui Ning ◽  
Xin-He Lou ◽  
Guo-Qiang Xu
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Intestinal Diseases ◽  
Inflammatory Bowel
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