Plumericin Protects against Experimental Inflammatory Bowel Disease by Restoring Intestinal Barrier Function and Reducing Apoptosis

Plumericin was evaluated for its ability to improve barrier function and to reduce apoptotic parameters during inflammation, both in intestinal epithelial cells, and in an animal experimental model of 2, 4, 6-dinitrobenzene sulfonic acid-induced colitis.
[Biomedicines]
Rapa, S. F., Di Paola, R., Cordaro, M., Siracusa, R., D’Amico, R., Fusco, R., Autore, G., Cuzzocrea, S., Stuppner, H., & Marzocco, S. (2021). Plumericin Protects against Experimental Inflammatory Bowel Disease by Restoring Intestinal Barrier Function and Reducing Apoptosis. Biomedicines, 9(1), 67. https://doi.org/10.3390/biomedicines9010067 Cite
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The Role of the Hippo Pathway in the Pathogenesis of Inflammatory Bowel Disease

The authors summarize the latest scientific literature on the involvement of this pathway in inflammatory bowel disease (IBD) from the following perspectives that account for the IBD pathogenesis: intestinal epithelial cell regeneration, immune regulation, gut microbiota, and angiogenesis.
[Cell Death & Disease]
Xie, Z., Wang, Y., Yang, G., Han, J., Zhu, L., Li, L., & Zhang, S. (2021). The role of the Hippo pathway in the pathogenesis of inflammatory bowel disease. Cell Death & Disease, 12(1), 1–14. https://doi.org/10.1038/s41419-021-03395-3 Cite
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Induced Organoids Derived from Patients with Ulcerative Colitis Recapitulate Colitic Reactivity

Researchers took advantage of induced pluripotent stem cells to develop an induced human UC-derived organoid model and compared it with the induced human normal organoid model.
[Nature Communications]
Sarvestani, S. K., Signs, S., Hu, B., Yeu, Y., Feng, H., Ni, Y., Hill, D. R., Fisher, R. C., Ferrandon, S., DeHaan, R. K., Stiene, J., Cruise, M., Hwang, T. H., Shen, X., Spence, J. R., & Huang, E. H. (2021). Induced organoids derived from patients with ulcerative colitis recapitulate colitic reactivity. Nature Communications, 12(1), 262. https://doi.org/10.1038/s41467-020-20351-5 Cite
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Landos Biopharma Announces Positive Results from a Phase 2 Trial of Oral BT-11 for Patients with Ulcerative Colitis

Landos Biopharma, announced positive results from a first-in-patients 12-week Phase II proof-of-concept trial of BT-11, a novel, orally administered, gut-restricted LANCL2 modulator in patients with mild to moderate ulcerative colitis. By activating the LANCL2 pathway and modulating the interactions between immunological and metabolic signals in immune cells, BT-11 is designed to create a favorable regulatory microenvironment in the gut.
[Landos Biopharma]
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Organoid-Based Models to Study the Role of Host-Microbiota Interactions in IBD

Scientists review different organoid-based ex vivo models that are currently available, and benchmark their suitability and limitations for specific research questions.
[Journal of Crohns & Colitis]
Poletti, M., Arnauts, K., Ferrante, M., & Korcsmaros, T. (2020). Organoid-based models to study the role of host-microbiota interactions in IBD. Journal of Crohn’s and Colitis, jjaa257. https://doi.org/10.1093/ecco-jcc/jjaa257 Cite
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Colonic Epithelial-Derived Selenoprotein P Is the Source for Antioxidant-Mediated Protection in Colitis-Associated Cancer

Scientists sought to delineate tissue-specific contributions of Selenoprotein P (SELENOP) to intestinal inflammatory carcinogenesis and define clinical context. SELENOP loss was assessed in human ulcerative colitis organoids, and expression was queried in human and adult UC samples.
[Gastroenterology]
Colonic epithelial-derived Selenoprotein P is the source for antioxidant-mediated protection in colitis-associated cancer - Gastroenterology. (n.d.). Retrieved January 5, 2021, from https://www.gastrojournal.org/article/S0016-5085(20)35623-7/pdf?referrer=https%3A%2F%2Fpubmed.ncbi.nlm.nih.gov%2F Cite
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RNF186 Regulates EFNB1 (Ephrin B1)-EPHB2-Induced Autophagy in the Colonic Epithelial Cells for the Maintenance of Intestinal Homeostasis

Researchers demonstrated an important role for RNF186 in macroautophagy/autophagy activation in colonic epithelial cells and intestinal homeostasis. Mechanistically, RNF186 acts as an E3 ubiquitin-protein ligase for EPHB2 and regulates the ubiquitination of EPHB2.
[Autophagy]
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Bacainn Therapeutics Reports Positive Topline Results from Phase I Study of BT051, a Novel Therapeutic Approach to Treat Inflammatory Diseases Such As Ulcerative Colitis

Bacainn Therapeutics, Inc. announced the successful completion of the company’s Phase I, first-in-human clinical trial of BT051, a novel, orally administered, gut-selective inhibitor of migration and activation of neutrophils.
[Bacainn Therapeutics, Inc. (Business Wire, Inc.)]
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A Critical Role of Endothelial Cell Protein C Receptor in the Intestinal Homeostasis in Experimental Colitis

Investigators report that endothelial cell protein C receptor was expressed in the colon epithelial cells, CD11c+, and CD21+/CD35+ myeloid cells surrounding the crypts in the colon mucosa.
[Scientific Reports]
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The Roles and Functions of Paneth Cells in Crohn’s Disease: A Critical Review

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.
[Cell Proliferation]
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NDRG2 Regulates Adherens Junction Integrity to Restrict Colitis and Tumourigenesis

Intestine-specific Ndrg2 deficiency mice were subjected to DSS- or TNBS-induced colitis, and AOM-DSS-induced colitis-associated tumour. HT29 cells, Caco2 cells, primary intestinal epithelial cells from Ndrg2ΔIEC mice, mouse embryo fibroblasts from systemic Ndrg2 knockout mice, HEK293 cells and human UC and DC specimens were used to investigate NDRG2 function in colitis and colitis-associated tumour.
[EBioMedicine]
Wei, M., Ma, Y., Shen, L., Xu, Y., Liu, L., Bu, X., Guo, Z., Qin, H., Li, Z., Wang, Z., Wu, K., Yao, L., Li, J., & Zhang, J. (2020). NDRG2 regulates adherens junction integrity to restrict colitis and tumourigenesis. EBioMedicine, 61. https://doi.org/10.1016/j.ebiom.2020.103068 Cite
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