The complement-activated product, complement component 5a (C5a), is a potent inflammatory peptide with a broad spectrum of functions. In vivo and in vitro studies have demonstrated that C5a serves an important role in inflammation; however, the role of C5a in the pathogenesis of inflammatory bowel disease (IBD) is not known. The purpose of the current study was to investigate the role of C5a in IBD using an experimental mouse model of colitis. Colitis was induced in mice using 2,4,6-trinitrobenzene sulfonic acid (TNBS), and C5a aptamers were subsequently administered via intraperitoneal injection. Clinical symptoms of the disease, histopathological analysis of the colon and the level of inflammatory components were examined. The symptoms of colitis, including changes in behavior, weight loss, colon damage and an increase in inflammatory cytokines, were attenuated following the treatment of mice with TNBS-induced colitis with C5a aptamers. The aptamer-treated mice exhibited a marked attenuation of colitis when compared with untreated mice, as demonstrated by the phenotypic observations, histological examinations and inflammatory cytokine levels. Colitis is characterized by an imbalance between pro-inflammatory and anti-inflammatory mediators. The results of the current study suggest that C5a may serve a critical role in inflammation in IBD.
[1]Acad Mil Med Sci, Mil Vet Inst, Key Lab Jilin Prov Zoonosis Prevent & Control, 666 Liuying West Rd, Changchun 130000, Jilin, Peoples R China.
[2]Jilin Univ, Dept Rheumatol, Hosp 1, 71 Xinmin St, Changchun 130021, Jilin, Peoples R China.
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