The immune-stimulating peptide WKYMVm has therapeutic effects against ulcerative colitis.
- Author:
Sang Doo KIM
1
;
Soonil KWON
;
Sung Kyun LEE
;
Minsoo KOOK
;
Ha Young LEE
;
Ki Duk SONG
;
Hak Kyo LEE
;
Suk Hwan BAEK
;
Chan Bae PARK
;
Yoe Sik BAE
Author Information
1. Department of Biological Science, Sungkyunkwan University, Suwon, Korea. yoesik@skku.edu
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
therapeutics;
ulcerative colitis;
WKYMVm
- MeSH:
Adjuvants, Immunologic/pharmacology/*therapeutic use;
Animals;
Caco-2 Cells;
Cell Proliferation;
Colitis, Ulcerative/*drug therapy/metabolism;
Colon/pathology;
Humans;
Interleukin-23/genetics/metabolism;
Intestinal Mucosa/drug effects/metabolism/pathology;
Mice;
Mice, Inbred C57BL;
Oligopeptides/pharmacology/*therapeutic use;
Permeability;
Receptors, Formyl Peptide/antagonists & inhibitors;
Transforming Growth Factor beta/genetics/metabolism
- From:Experimental & Molecular Medicine
2013;45(9):e40-
- CountryRepublic of Korea
- Language:English
-
Abstract:
In this study, we examined the therapeutic effects of an immune-stimulating peptide, WKYMVm, in ulcerative colitis. The administration of WKYMVm to dextran sodium sulfate (DSS)-treated mice reversed decreases in body weight, bleeding score and stool score in addition to reversing DSS-induced mucosa destruction and shortened colon. The WKYMVm-induced therapeutic effect against ulcerative colitis was strongly inhibited by a formyl peptide receptor (FPR) 2 antagonist, WRWWWW, indicating the crucial role of FPR2 in this effect. Mechanistically, WKYMVm effectively decreases intestinal permeability by stimulating colon epithelial cell proliferation. WKYMVm also strongly decreases interleukin-23 and transforming growth factor-beta production in the colon of DSS-treated mice. We suggest that the potent immune-modulating peptide WKYMVm and its receptor FPR2 may be useful in the development of efficient therapeutic agents against chronic intestinal inflammatory diseases.