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Crohn's disease

An Insight into the Roles of Dietary Tryptophan and Its Metabolites in Intestinal Inflammation and Inflammatory Bowel Disease

[Molecular Nutrition & Food Research] The authors discuss the complex mechanisms and interrelationships of the three major metabolic pathways of Trp in regulating inflammation, which could elucidate the value of dietary Trp to be used as a nutrient for IBD patients.

Interleukin-28A Induces Epithelial Barrier Dysfunction in CD Patient-derived Intestinal Organoids

[American Journal of Physiology-Gastrointestinal and Liver Physiology] Crohn's disease patient-derived intestinal organoids were characterized by differentiation gene markers and then exposed to TNF-α, IFN-γ, IL-1β or LPS, or IL-28A with or without GLPG0634.

From Inflammation to Colitis-Associated Colorectal Cancer in Inflammatory Bowel Disease: Pathogenesis and Impact of Current Therapies

[Digestive and Liver Disease] Scientists present an overview of the current knowledge of colitis-associated cancer (CAC) in inflammatory bowel disease (IBD) patients, focusing on the role of inflammation in the pathogenesis of CAC and the potential for IBD drugs to interfere with the process of carcinogenesis by reducing the inflammatory process or by modulating pathways directly involved in carcinogenesis.

The Roles and Functions of Paneth Cells in Crohn’s Disease: A Critical Review

[Cell Proliferation] Paneth cells are located at the base of small intestinal crypts and secrete the α‐defensins, human α‐defensin 5 and human α‐defensin 6 in response to bacterial, cholinergic and other stimuli.

Monocytes from Infliximab-Resistant Patients with Crohn’s Disease Exhibit a Disordered Cytokine Profile

[Scientific Reports] Investigators compared the inflammatory phenotype of monocytes from Crohn's disease patients, who responded or non-responded to infliximab. Under basal conditions, the mRNA for the cytokines TNFα, IL-23, IL-1β and the chemokines CXCL8/IL-8, CCL5/RANTES and CCL2/MCP-1 was up-regulated in monocytes from non-responders than responders.

AXL Is a Potential Target for the Treatment of Intestinal Fibrosis

[Inflammatory Bowel Diseases] This study demonstrated that inhibition of AXL signaling with the small molecule inhibitor BGB324 abrogated both matrix-stiffness and transforming growth factor beta–induced fibrogenesis in human colonic myofibroblasts.

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