scholarly journals A review of the efficacy of dietary polyphenols in experimental models of inflammatory bowel diseases

2015 ◽  
Vol 6 (6) ◽  
pp. 1773-1786 ◽  
Author(s):  
Derek A. Martin ◽  
Bradley W. Bolling
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Experimental Models ◽  
Rodent Models ◽  
Dietary Polyphenols ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Higher Doses

The use of polyphenols in rodent models of inflammatory bowel diseases is reviewed. Many polyphenols inhibit colitis through multiple mechanisms, however higher doses of some treatments may exacerbate inflammation.

scholarly journals The Role of Carrageenan in Inflammatory Bowel Diseases and Allergic Reactions: Where Do We Stand?

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3402
Author(s):  
Barbara Borsani ◽  
Raffaella De Santis ◽  
Veronica Perico ◽  
Francesca Penagini ◽  
Erica Pendezza ◽  
...  
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Experimental Models ◽  
Gelling Agent ◽  
Current Evidence ◽  
Allergic Reactions ◽  
Processed Foods ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Carrageenan (CGN) is a high molecular weight polysaccharide extracted from red seaweeds, composed of D-galactose residues linked in β-1,4 and α-1,3 galactose-galactose bond, widely used as a food additive in processed foods for its properties as a thickener, gelling agent, emulsifier, and stabilizer. In recent years, with the spread of the Western diet (WD), its consumption has increased. Nonetheless, there is a debate on its safety. CGN is extensively used as an inflammatory and adjuvant agent in vitro and in animal experimental models for the investigation of immune processes or to assess the activity of anti-inflammatory drugs. CGN can activate the innate immune pathways of inflammation, alter the gut microbiota composition and the thickness of the mucus barrier. Clinical evidence suggests that CGN is involved in the pathogenesis and clinical management of inflammatory bowel diseases (IBD), indeed food-exclusion diets can be an effective therapy for disease remission. Moreover, specific IgE to the oligosaccharide α-Gal has been associated with allergic reactions commonly referred to as the “α-Gal syndrome”. This review aims to discuss the role of carrageenan in inflammatory bowel diseases and allergic reactions following the current evidence. Furthermore, as no definitive data are available on the safety and the effects of CGN, we suggest gaps to be filled and advise to limit the human exposure to CGN by reducing the consumption of ultra-processed foods.

scholarly journals Advances in the understanding of mineral and bone metabolism in inflammatory bowel diseases

2011 ◽  
Vol 300 (2) ◽  
pp. G191-G201 ◽  
Author(s):  
Fayez K. Ghishan ◽  
Pawel R. Kiela
Keyword(s):  
Vitamin D ◽  
Bone Metabolism ◽  
Inflammatory Mediators ◽  
Inflammatory Bowel Diseases ◽  
Experimental Models ◽  
Mineral Density ◽  
Anabolic Hormone ◽  
Increased Risk ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Chronic inflammatory disorders such as inflammatory bowel diseases (IBDs) affect bone metabolism and are frequently associated with the presence of osteopenia, osteoporosis, and increased risk of fractures. Although several mechanisms may contribute to skeletal abnormalities in IBD patients, inflammation and inflammatory mediators such as TNF, IL-1β, and IL-6 may be the most critical. It is not clear whether the changes in bone metabolism leading to decreased mineral density are the result of decreased bone formation, increased bone resorption, or both, with varying results reported in experimental models of IBD and in pediatric and adult IBD patients. New data, including our own, challenge the conventional views, and contributes to the unraveling of an increasingly complex network of interactions leading to the inflammation-associated bone loss. Since nutritional interventions (dietary calcium and vitamin D supplementation) are of limited efficacy in IBD patients, understanding the pathophysiology of osteopenia and osteoporosis in Crohn's disease and ulcerative colitis is critical for the correct choice of available treatments or the development of new targeted therapies. In this review, we discuss current concepts explaining the effects of inflammation, inflammatory mediators and their signaling effectors on calcium and phosphate homeostasis, osteoblast and osteoclast function, and the potential limitations of vitamin D used as an immunomodulator and anabolic hormone in IBD.

scholarly journals Innate Lymphoid Cells as Regulators of Epithelial Integrity: Therapeutic Implications for Inflammatory Bowel Diseases

2021 ◽  
Vol 8 ◽  
Author(s):  
Anja Schulz-Kuhnt ◽  
Markus F. Neurath ◽  
Stefan Wirtz ◽  
Imke Atreya
Keyword(s):  
Epithelial Cell ◽  
Immune Cells ◽  
Inflammatory Bowel Diseases ◽  
Innate Lymphoid Cells ◽  
Experimental Models ◽  
Lymphoid Cells ◽  
Intestinal Epithelial ◽  
Epithelial Integrity ◽  
Bowel Diseases ◽  
Inflammatory Bowel

The occurrence of epithelial defects in the gut relevantly contributes to the pathogenesis of inflammatory bowel diseases (IBD), whereby the impairment of intestinal epithelial barrier integrity seems to represent a primary trigger as well as a disease amplifying consequence of the chronic inflammatory process. Besides epithelial cell intrinsic factors, accumulated and overwhelmingly activated immune cells and their secretome have been identified as critical modulators of the pathologically altered intestinal epithelial cell (IEC) function in IBD. In this context, over the last 10 years increasing levels of attention have been paid to the group of innate lymphoid cells (ILCs). This is in particular due to a preferential location of these rather newly described innate immune cells in close proximity to mucosal barriers, their profound capacity to secrete effector cytokines and their numerical and functional alteration under chronic inflammatory conditions. Aiming on a comprehensive and updated summary of our current understanding of the bidirectional mucosal crosstalk between ILCs and IECs, this review article will in particular focus on the potential capacity of gut infiltrating type-1, type-2, and type-3 helper ILCs (ILC1s, ILC2s, and ILC3s, respectively) to impact on the survival, differentiation, and barrier function of IECs. Based on data acquired in IBD patients or in experimental models of colitis, we will discuss whether the different ILC subgroups could serve as potential therapeutic targets for maintenance of epithelial integrity and/or mucosal healing in IBD.

The value of experimental models of colitis in predicting efficacy of biological therapies for inflammatory bowel diseases

2013 ◽  
Vol 305 (11) ◽  
pp. G763-G785 ◽  
Author(s):  
Vassilis Valatas ◽  
Michael Vakas ◽  
George Kolios
Keyword(s):  
Animal Models ◽  
Inflammatory Bowel Diseases ◽  
Inflammatory Diseases ◽  
Experimental Models ◽  
Biological Therapies ◽  
Disease Pathogenesis ◽  
Preclinical Data ◽  
Bowel Diseases ◽  
Inflammatory Bowel

During the last decade, biological therapies have an increasing share in the modern therapeutics of various diseases including inflammatory bowel diseases (IBD). Animal models of IBD have often been used to identify the targets of biological therapies, to test their relevance to disease pathogenesis, to assess their therapeutic efficacy in vivo, and to check for drug toxicity. In the field of inflammatory diseases the majority of biologics under development have failed to reach the clinic. This review examines the ability of preclinical data from animal models of IBD to predict success or failure of biologics in human IBD. Specifically, it describes the murine models of IBD, the mechanism of disease induction, the phenotype of the disease, its relevance to human IBD, and the specific immunological features of disease pathogenesis in each model and mainly compares the results of the phase II and III trials of biologics in IBD with preclinical data obtained from studies in animal models. Finally, it examines the possible reasons for low success in translation from bench to bedside and offers some suggestions to improve translation rates.

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