The authors analyzed the CXCL8-CXCR1/2 axis related signaling pathways and ncRNAs in ulcerative colitis (UC), as well as recent advances in our understanding of the CXCL8-CXCR1/2 axis inhibition as a therapeutic strategy against UC.
[Biomedicine & Pharmacotherapy]
Scientists give an overview of the differentiation between ileal and colonic Crohn’s disease using data in the context of epidemiology, genetics, macroscopic differences such as creeping fat and histological findings.
[Nature Reviews Gastroenterology & Hepatology]
Mechanistically, plectin deficiency in intestinal epithelial cell led to aberrant keratin filament network organization and the formation of dysfunctional hemidesmosomes and intercellular junctions.
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Krausova, A., Buresova, P., Sarnova, L., Oyman-Eyrilmez, G., Skarda, J., Wohl, P., Bajer, L., Sticova, E., Bartonova, L., Pacha, J., Koubkova, G., Prochazka, J., Spörrer, M., Dürrbeck, C., Stehlikova, Z., Vit, M., Ziolkowska, N., Sedlacek, R., Jirak, D., … Gregor, M. (2021). Plectin ensures intestinal epithelial integrity and protects colon against colitis. Mucosal Immunology, 1–12. https://doi.org/10.1038/s41385-021-00380-z Cite
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.
[Molecular Nutrition & Food Research]
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Li, X., Zhang, Z.-H., Zabed, H. M., Yun, J., Zhang, G., & Qi, X. (2021). An Insight into the Roles of Dietary Tryptophan and Its Metabolites in Intestinal Inflammation and Inflammatory Bowel Disease. Molecular Nutrition & Food Research, 65(5), 2000461. https://doi.org/https://doi.org/10.1002/mnfr.202000461 Cite
IL-1β decreased the expression of the LXR target gene ABCA1 in cultured intestinal epithelial cells. The synthetic LXR agonist GW3965 led to a decreased nuclear positivity of the p65 subunit of nuclear factor kappa B, a phosphorylation ratio of the p44-42 mitogen-activated protein kinase, and the expression of CCL-28 and IL-8 in IL-1β-stimulated Caco-2 cells.
[Inflammatory Bowel Diseases]
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An in vitro model using human colon organoids was established by 60 weeks of inflammatory stimulation. The key gene for mucosal injury caused by long-term inflammation was identified by microarray analysis. An in vivo model was established by xenotransplantation of organoids into mouse colonic mucosa.
[Journal of Crohns & Colitis]
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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.
[Digestive and Liver Disease]
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Bristol Myers Squibb announced that the FDA has accepted its supplemental New Drug Application for Zeposia® for the treatment of adults with moderately to severely active ulcerative colitis.
[Bristol Myers Squibb]
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Scientists investigated the in vivo role of Dhx15 in intestinal antibacterial responses by generating mice that were intestinal epithelial cell-specific deficient for Dhx15.
[Proceedings of the National Academy of Sciences of the United States of America]
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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.
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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]
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