title: Possible role of mucosal mast cells in the recovery process of colitis induced by dextran sulfate sodium in rats.
abstract: To clarify the role of mucosal mast cells in the lesion sites of colitis induced by dextran sulfate sodium (DSS) in rats, we investigated the histological changes and alterations relevant to mucosal mast cells in the spontaneous recovery process of colitis. Oral administration of 4% DSS solution for 11 days resulted in surface epithelial loss, crypt loss and goblet cell depletion in the rectal mucosa. A marked infiltration of inflammatory cells into the mucosa, which was consistent with a significant increase in myeloperoxidase (MPO) activity, was observed. In addition, mucosal mast cell number and rat mast cell protease (RMCP) I and II levels in the rectum increased at day 0 after DSS treatment, and most of the mucosal mast cells were degranulated. After replacing 4% DSS solution with water, re-epithelialization and restoration of goblet cells were observed at day 5 and day 10, respectively, but crypt damage was hardly recovered even at day 20. The elevated myeloperoxidase activity was significantly decreased from day 5 after DSS treatment. The increased number of mucosal mast cells was further elevated up to about 1.5-fold at day 10 and day 20 after DSS treatment and little degranulation was observed. In the spontaneous recovery process, the increased rat mast cell protease II level in the rectum was maintained for 20 days, while the increased rat mast cell protease I level was gradually decreased and recovered to control level. These results suggest that proliferated mucosal mast cells remained for 20 days, although most of infiltrated inflammatory cells disappeared in spontaneous recovery process of colitis. It may therefore be presumed that proliferated mucosal mast cells play a role in spontaneous recovery process of the colitis induced by DSS.
authors.affiliation: Department of Clinical Biochemistry, Faculty of Pharmaceutical Sciences, Setsunan University, Hirakata 573-0101, Japan.
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Iba
authors.forename: Yukio
authors.initials: Y
authors.lastname: Sugimoto
authors.forename: Chiaki
authors.initials: C
authors.lastname: Kamei
authors.forename: Tohru
authors.initials: T
authors.lastname: Masukawa
mesh_terms: D000818:Animals; D002452:Cell Count; D053818:Chymases; D003092:Colitis / Q000139:chemically induced / Q000201:enzymology / Q000473:pathology*; D016264:Dextran Sulfate / Q000633:toxicity*; D004195:Disease Models, Animal; D007413:Intestinal Mucosa / Q000201:enzymology / Q000473:pathology*; D008297:Male; D008407:Mast Cells / Q000166:cytology / Q000201:enzymology*; D009195:Peroxidase / Q000378:metabolism; D011349:Proctitis / Q000139:chemically induced / Q000201:enzymology / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012007:Rectum / Q000201:enzymology / Q000473:pathology*; D012697:Serine Endopeptidases / Q000378:metabolism
chemical_list: D016264:Dextran Sulfate; D009195:Peroxidase; D012697:Serine Endopeptidases; C083294:chymase 2; D053818:Chymases