Role of intestinal subepithelial myofibroblasts in inflammation and regenerative response in the gut

Pharmacol Ther. 2007 Apr;114(1):94-106. doi: 10.1016/j.pharmthera.2006.12.004. Epub 2007 Jan 23.


Inflammatory bowel disease (IBD) is characterized by an ongoing mucosal inflammation caused by a dysfunctional host immune response to commensal microbiota and dietary factors. In the pathophysiology of IBD, mesenchymal cells such as intestinal subepithelial myofibroblasts (ISEMF) affect the recruitment, retention and activation of immune cells. Mesenchymal cells also promote resolution of inflammatory activity accompanied with balanced repair processes. The transient appearance of mesenchymal cells is a feature of normal wound healing, but the persistence of these cells is associated with tissue fibrosis. Recent studies suggest that mesenchymal cells derived from bone marrow (BM) stem cells play a crucial role in intestinal repair and fibrosis. This article focuses on recent knowledge about ISEMF in the field of immune response inflammation and repair. Two major topics were documented: interaction between interleukin (IL)-17-secreting CD4+ cells (Th-17 cells) and about role of BM-derived stem cells in mucosal regenerative response via differentiation to ISEMF. Recent therapeutic strategies targeting BM stem cells for IBD patients were also documented.

Publication types

  • Review

MeSH terms

  • Animals
  • Bone Marrow Cells / cytology
  • Extracellular Matrix / physiology
  • Fibroblasts / cytology
  • Fibroblasts / physiology*
  • Humans
  • Inflammation
  • Inflammatory Bowel Diseases / immunology
  • Inflammatory Bowel Diseases / therapy
  • Interleukin-17 / immunology
  • Intestinal Mucosa / cytology
  • Intestinal Mucosa / physiology*
  • Intestines / cytology
  • Intestines / physiology*
  • Matrix Metalloproteinases / metabolism
  • Regeneration
  • T-Lymphocytes, Helper-Inducer / immunology
  • Wnt Proteins / metabolism
  • beta Catenin / metabolism


  • Interleukin-17
  • Wnt Proteins
  • beta Catenin
  • Matrix Metalloproteinases