Colonic mucin release in response to immobilization stress is mast cell dependent

Am J Physiol. 1998 Jun;274(6):G1094-1100. doi: 10.1152/ajpgi.1998.274.6.G1094.


We recently reported that immobilization stress increased colonic motility, mucin, and prostaglandin E2 (PGE2) release and mucosal mast cell degranulation in rat colon [Proc. Natl. Acad. Sci. USA 93: 12611-12615, 1996; Am. J. Physiol. 271 (Gastrointest. Liver Physiol. 34): G884-G892, 1996]. To directly assess the contribution of mast cells, we compared colonic responses to stress in mast cell-deficient KitW/KitW-v and normal(+/+) mice. Mucin and PGE2 release were measured in colonic explants cultured from KitW/KitW-v and (+/+) mice 30 min after immobilization stress. We found that stress stimulated colonic mucin release (1.8-fold), goblet cell depletion (3-fold), and PGE2 (2.3-fold) release in (+/+) but not mast cell-deficient KitW/KitW-v mice. However, mast cell-deficient mice that had their mast cell population reconstituted by injection of bone marrow-derived mast cells from (+/+) mice had colonic responses to stress similar to those of normal (+/+) mice. In contrast, colonic transit changes in response to stress, estimated by fecal output, were similar between KitW/KitW-v and normal (+/+) mice. We conclude that mast cells regulate colonic mucin and PGE2 release but not colonic transit changes in response to immobilization stress.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Colon / metabolism*
  • Corticosterone / blood
  • Culture Techniques
  • Dinoprostone / metabolism
  • Gastrointestinal Motility
  • Male
  • Mast Cells / physiology*
  • Mice
  • Mice, Mutant Strains
  • Mucins / metabolism*
  • Restraint, Physical
  • Stress, Physiological / physiopathology*


  • Mucins
  • Dinoprostone
  • Corticosterone