Published online May 28, 2015. doi: 10.3748/wjg.v21.i20.6157
Peer-review started: July 26, 2014
First decision: September 27, 2014
Revised: November 10, 2014
Accepted: December 20, 2014
Article in press: December 22, 2014
Published online: May 28, 2015
Processing time: 309 Days and 2.8 Hours
AIM: To evaluate the efficacy of the improved thrombospondin mimetic peptide ABT-898 in a murine model of ulcerative colitis.
METHODS: The dextran sodium sulfate (DSS) was used for the induction of colitis in both TSP-1 deficient (TSP-1-/-) and wild type (WT) mice during 7 d. While mice were receiving the DSS dissolved in the drinking water, the ABT-898 peptide was dissolved in sterile 5% glucose solution and delivered using mini pumps subcutaneously implanted. Plasma samples were analyzed for interleukin (IL)-6 by ELISA assay and colonic tissues were harvested, fixed and processed for histological evaluation. Immunohistochemistry using antibodies for the detection of CD31 and MECA in endothelial cells was performed. Inflammation was graded in colonic sections and the number of microvessels in each lesion was assessed. Activation of signal transducer and activator of transcription 3 (STAT3) in colonic samples was quantified by immunohistochemistry and Western blotting using antibodies against total STAT3 and phosphorylated STAT3 (pSTAT3) (Ser727).
RESULTS: Treatment with ABT-898 considerably diminished the inflammatory response in WT and TSP-1-/- mice (P < 0.0001 in both groups vs control). Identification of blood vessels highlighted by CD31/MECA immunohistochemistry, showed significantly reduced vessel counts in colitic lesions of WT and TSP-1-/- mice treated with ABT898 (TSP-1-/- controls/TSP-1-/- treated, P = 0.0002; WT controls/WT treated, P = 0.0005). Consistently, IL-6 was significantly diminished in plasma samples of TSP-1-/- and WT treated with the peptide when compared to the control mice (P = 0.0002 and P = 0.0148, respectively). pSTAT3 positive cells were quantified in WT and TSP-1-/- treated with ABT-898. A significant decrease in positive cells for pSTAT3 was observed in treated mice (TSP-1-/- controls/TSP-1-/- treated, P = 0.0089; WT/WT treated, P = 0.0110). These results were confirmed by Western blotting analyses showing lower levels of pSTAT3 in colitic lesions from mice treated with the peptide ABT-898.
CONCLUSION: These findings indicate that the new peptide ABT-898 ameliorates inflammation and angiogenesis and might be a therapeutic alternative in IBD and inflammatory diseases.
Core tip: Inflammatory bowel disease is still incurable and a major burden in the patient’s life and health care system. The discovery of new and safe therapeutic alternatives is urgently needed. This study tested the efficacy of a new thrombospondin- derived peptide, ABT-898 in a murine model of colitis. Our results indicate that this peptide was able to ameliorate inflammation and angiogenesis. In addition, mice treated with ABT-898 showed significant decrease of plasmatic Interleukin-6 and lesser activation of signal transducer and activator of transcription 3 in colitic lesions. These findings suggest that ABT-898 may indeed be an alternative treatment for inflammatory bowel disease.