The role of innate immune-stimulated epithelial apoptosis during gastrointestinal inflammatory diseases

Richard H. Siggers, David J. Hackam

Research output: Contribution to journalReview articlepeer-review

Abstract

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.

Original languageEnglish (US)
Pages (from-to)3623-3634
Number of pages12
JournalCellular and Molecular Life Sciences
Volume68
Issue number22
DOIs
StatePublished - Nov 2011
Externally publishedYes

Keywords

  • Chron's disease
  • Intestininal inflammation
  • Necrotizing enterocolitis
  • TLR4
  • Ulcerative colitis

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology
  • Pharmacology
  • Cellular and Molecular Neuroscience
  • Cell Biology

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