mp5b00069_si_001.pdf (930.28 kB)
Cathelicidin-BF, a Novel Antimicrobial Peptide from Bungarus fasciatus, Attenuates Disease in a Dextran Sulfate Sodium Model of Colitis
journal contribution
posted on 2015-05-04, 00:00 authored by Haiwen Zhang, Xi Xia, Feifei Han, Qin Jiang, Yili Rong, Deguang Song, Yizhen WangAntimicrobial peptides are molecules
of innate immunity. Cathelicidin-BF
is the first cathelicidin peptide found in reptiles. However, the
immunoregulatory and epithelial barrier protective properties of C-BF
have not been reported. Inflammatory bowel diseases, including ulcerative
colitis and Crohn’s disease, can lead to colon cancer, the
third most common malignant tumor. The objective is to develop the
new found cathelicidin-BF as a therapeutic to patients of ulcerative
colitis. The morphology of the colon epithelium was observed by H&E
staining; apoptosis index and infiltration of inflammatory cells in
colonic epithelium were measured by TUNEL and immunohistochemistry;
the expression level of endogenous mCRAMP was analyzed by immunofluorescence;
and phosphorylation of the transcription factors c-jun and NF-κB
in colon were analyzed by Western blot. Our results showed that the
morphology of the colon epithelium in the C-BF+DSS group was improved
compared with the DSS group. Apoptosis and infiltration of inflammatory
cells in colonic epithelium were also significantly attenuated in
the C-BF+DSS group compared with the DSS group, and the expression
level of endogenous mCRAMP in the DSS group was significantly higher
than other groups. DSS-induced phosphorylation level of c-jun and
NF-κB while C-BF effectively inhibited phosphorylation of NF-κB
(p65). The barrier protective effect of C-BF was still excellent.
In conclusion, C-BF effectively attenuated inflammation and improved
disrupted barrier function. Notably, this is the first report to demonstrate
that C-BF attenuates DSS-induced UC both through the regulation of
intestinal immune and retention of barrier function, and the exact
pathway was through NF-κB.