The latest study from the Jill Roberts Institute, "The neuropeptide neuromedin U stimulates innate lymphoid cells and type 2 inflammation," was published on September 6 in Nature. To read more, click here.     Dr. Gregory Sonnenberg wins inaugural award from the Society for Mucosal Immunology. To read more, click here.  The Kenneth Rainin Foundation awarded Dr. Iliyan Iliev and colleagues from Mount Sinai a $250,000 Synergy Award to examine the composition of the fungal community in babies born to mothers with inflammatory bowel disease. To read more, click here. Dr. Randy Longman received the Irma T. Hirschl Career Scientist Award and the New York Crohn’s Foundation Award.    

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Death in the intestinal epithelium-basic biology and implications for inflammatory bowel disease.

TitleDeath in the intestinal epithelium-basic biology and implications for inflammatory bowel disease.
Publication TypeJournal Article
Year of Publication2016
AuthorsJ Blander, M
JournalFEBS J
Volume283
Issue14
Pagination2720-30
Date Published2016 Jul
ISSN1742-4658
Abstract

Every 4-5 days, intestinal epithelial cells (IEC) are terminated as they reach the end of their life. This process ensures that the epithelium is comprised of the fittest cells that maintain an impermeable barrier to luminal contents and the gut microbiota, as well as the most metabolically able cells that conduct functions in nutrient absorption, digestion, and secretion of antimicrobial peptides. IEC are terminated by apical extrusion-or shedding-from the intestinal epithelial monolayer into the gut lumen. Whether death by apoptosis signals extrusion or death follows expulsion by younger IEC has been a matter of debate. Seemingly a minor detail, IEC death before or after apical extrusion bears weight on the potential contribution of apoptotic IEC to intestinal homeostasis as a consequence of their recognition by intestinal lamina propria phagocytes. In inflammatory bowel disease (IBD), excessive death is observed in the ileal and colonic epithelium. The precise mode of IEC death in IBD is not defined. A highly inflammatory milieu within the intestinal lamina propria, rich in the proinflammatory cytokine, TNF-α, increases IEC shedding and compromises barrier integrity fueling more inflammation. A milestone in the treatment of IBD, anti-TNF-α therapy, may promote mucosal healing by reversing increased and inflammation-associated IEC death. Understanding the biology and consequences of cell death in the intestinal epithelium is critical to the design of new avenues for IBD therapy.

DOI10.1111/febs.13771
Alternate JournalFEBS J.
PubMed ID27250564
PubMed Central IDPMC4956528
Grant ListP01 DK072201 / DK / NIDDK NIH HHS / United States
R01 AI073899 / AI / NIAID NIH HHS / United States
R01 AI095245 / AI / NIAID NIH HHS / United States
R01 AI123284 / AI / NIAID NIH HHS / United States