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Article: A new role for cathelicidin in ulcerative colitis in mice

TitleA new role for cathelicidin in ulcerative colitis in mice
Authors
KeywordsAntimicrobial peptide
IBD
mCRAMP
Mucus
Issue Date2007
PublisherSociety for Experimental Biology and Medicine. The Journal's web site is located at http://www.ebmonline.org/
Citation
Experimental Biology And Medicine, 2007, v. 232 n. 6, p. 799-808 How to Cite?
AbstractCathelicidin, an antimicrobial peptide of the innate immune system, modulates microbial growth, wound healing, and inflammation. However, its association with inflammatory bowel diseases (IBDs) is unknown. Our objective was to determine whether cathelicidin would exert a modulatory effect on the progression of IBD and, if so, investigate the mechanism of action through which this effect occurred. We evaluated the potential for a synthetic cathelicidin, the mouse cathelin-related antimicrobial peptide (mCRAMP), to prevent the initiation and promote the healing of lesions from inflammatory colitis that was experimentally induced in mice with dextran sulfate sodium (DSS). During the experiment, mCRAMP was given: (i) as a parallel treatment starting together with 3% DSS feeding, and (ii) as a posttreatment starting 7 days after 3% DSS feeding. The body weight, fecal microflora populations, clinical symptoms, and histologic findings of colonic tissues were measured. Relative gene expression of mucins (MUC1, MUC2, MUC3, and MUC4) in colonic tissues was determined by real-time polymerase chain reaction. Intrarectal administration of mCRAMP ameliorated DSS-induced colitis with negligible effects on mucosal healing. The peptide also significantly reduced the increased number of fecal microflora in colitis animals. It reversed the decline of colonic mucus thickness during colitis through upregulation of the expression of mucin genes. Treatment with mCRAMP also prevented colitis development by suppressing the induction of apoptosis by DSS. The current study demonstrates for the first time that intrarectal administration of cathelicidin may be a novel therapeutic option for IBDs. Copyright © 2007 by the Society for Experimental Biology and Medicine.
Persistent Identifierhttp://hdl.handle.net/10722/80271
ISSN
2023 Impact Factor: 2.8
2023 SCImago Journal Rankings: 0.850
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTai, EKKen_HK
dc.contributor.authorWu, WKKen_HK
dc.contributor.authorWong, HPSen_HK
dc.contributor.authorLam, EKYen_HK
dc.contributor.authorYu, Len_HK
dc.contributor.authorCho, CHen_HK
dc.date.accessioned2010-09-06T08:04:26Z-
dc.date.available2010-09-06T08:04:26Z-
dc.date.issued2007en_HK
dc.identifier.citationExperimental Biology And Medicine, 2007, v. 232 n. 6, p. 799-808en_HK
dc.identifier.issn1535-3702en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80271-
dc.description.abstractCathelicidin, an antimicrobial peptide of the innate immune system, modulates microbial growth, wound healing, and inflammation. However, its association with inflammatory bowel diseases (IBDs) is unknown. Our objective was to determine whether cathelicidin would exert a modulatory effect on the progression of IBD and, if so, investigate the mechanism of action through which this effect occurred. We evaluated the potential for a synthetic cathelicidin, the mouse cathelin-related antimicrobial peptide (mCRAMP), to prevent the initiation and promote the healing of lesions from inflammatory colitis that was experimentally induced in mice with dextran sulfate sodium (DSS). During the experiment, mCRAMP was given: (i) as a parallel treatment starting together with 3% DSS feeding, and (ii) as a posttreatment starting 7 days after 3% DSS feeding. The body weight, fecal microflora populations, clinical symptoms, and histologic findings of colonic tissues were measured. Relative gene expression of mucins (MUC1, MUC2, MUC3, and MUC4) in colonic tissues was determined by real-time polymerase chain reaction. Intrarectal administration of mCRAMP ameliorated DSS-induced colitis with negligible effects on mucosal healing. The peptide also significantly reduced the increased number of fecal microflora in colitis animals. It reversed the decline of colonic mucus thickness during colitis through upregulation of the expression of mucin genes. Treatment with mCRAMP also prevented colitis development by suppressing the induction of apoptosis by DSS. The current study demonstrates for the first time that intrarectal administration of cathelicidin may be a novel therapeutic option for IBDs. Copyright © 2007 by the Society for Experimental Biology and Medicine.en_HK
dc.languageengen_HK
dc.publisherSociety for Experimental Biology and Medicine. The Journal's web site is located at http://www.ebmonline.org/en_HK
dc.relation.ispartofExperimental Biology and Medicineen_HK
dc.subjectAntimicrobial peptideen_HK
dc.subjectIBDen_HK
dc.subjectmCRAMPen_HK
dc.subjectMucusen_HK
dc.titleA new role for cathelicidin in ulcerative colitis in miceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1535-3702&volume=232&spage=799&epage=808&date=2007&atitle=A+new+role+for+cathelicidin+in+ulcerative+colitis+in+miceen_HK
dc.identifier.emailWong, HPS:hpswong@hkusua.hku.hken_HK
dc.identifier.authorityWong, HPS=rp00808en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid17526772-
dc.identifier.scopuseid_2-s2.0-34249739104en_HK
dc.identifier.hkuros157305en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34249739104&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume232en_HK
dc.identifier.issue6en_HK
dc.identifier.spage799en_HK
dc.identifier.epage808en_HK
dc.identifier.isiWOS:000246828100011-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTai, EKK=9842278900en_HK
dc.identifier.scopusauthoridWu, WKK=8507784700en_HK
dc.identifier.scopusauthoridWong, HPS=8644138100en_HK
dc.identifier.scopusauthoridLam, EKY=8644138600en_HK
dc.identifier.scopusauthoridYu, L=16314581700en_HK
dc.identifier.scopusauthoridCho, CH=14067000400en_HK
dc.identifier.issnl1535-3699-

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