Journal
CELLULAR AND MOLECULAR LIFE SCIENCES
Volume 68, Issue 22, Pages 3623-3634Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00018-011-0821-4
Keywords
Intestininal inflammation; Necrotizing enterocolitis; Chron's disease; Ulcerative colitis; TLR4
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Funding
- NIDDK NIH HHS [R01 DK083752] Funding Source: Medline
- NIGMS NIH HHS [P50 GM053789, R01 GM078238] Funding Source: Medline
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The maintenance of mucosal barrier equilibrium in the intestine requires a delicate and dynamic balance between enterocyte loss by apoptosis and the generation of new cells by proliferation from stem cell precursors at the base of the intestinal crypts. When the balance shifts towards either excessive or insufficient apoptosis, a broad range of gastrointestinal diseases can manifest. Recent work from a variety of laboratories has provided evidence in support of a role for receptors of the innate immune system, including Toll-like receptors 2, 4, and 9 as well as the intracellular pathogen recognition receptor NOD2/CARD15, in the initiation of enterocyte apoptosis. The subsequent induction of enterocyte apoptosis in response to the activation of these innate immune receptors plays a key role in the development of various intestinal diseases, including necrotizing enterocolitis, Crohn's disease, ulcerative colitis, and intestinal cancer. This review will detail the regulatory pathways that govern enterocyte apoptosis, and will explore the role of the innate immune system in the induction of enterocyte apoptosis in gastrointestinal disease.
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