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Published on: March 10, 2015
Therapeutic potential of follistatin for colonic inflammation in mice
Taeko Dohi1, Chieko Ejima, Rie Kato
1Department of Gastroenterology, Research Institute, International Medical Center of Japan, Tokyo. dohi@ri.imcj.go.jp
Background And Aims:
Activins belong to the transforming growth factor-beta superfamily. Recent studies have shown that activin and its natural antagonist, follistatin, are involved in tissue repair and inflammatory processes. The aim of this study was to determine whether neutralization of activins with follistatin would have an in vivo anti-inflammatory effect in several murine models of colitis.
Methods:
We assessed activin levels in the colitis induced by intracolonic administration of trinitrobenzene sulfonic acid (TNBS). We subsequently tested the effects of an intraperitoneal injection of follistatin before or after induction of TNBS colitis. We also examined the established colitis induced by oral dextran sulfate sodium (DSS) as well as the spontaneous colitis that develops in interleukin (IL)-10 gene-deficient (IL-10 -/- ) mice.
Results:
Levels of activin transcripts in the colon during the acute phase of TNBS colitis were up-regulated. Epithelial cells, infiltrating macrophages (Mvarphi), and endothelial cells produced excess activin betaA. Pretreatment with follistatin increased the survival rate of mice with TNBS colitis from 33% to 82% and decreased the plasma levels of IL-6 and amyloid A. Administration of follistatin also reduced the histologic score and tissue myeloperoxidase activity in established TNBS and DSS colitis and reduced the severity of the colitis in IL-10 -/- mice. Based on results obtained from 3 mouse models and from in vitro experiments, follistatin promoted the proliferation of colonic epithelial cells.
Conclusions:
Neutralization of activins by follistatin promoted epithelial cell division and tissue repair, clearly suggesting a treatment modality for intestinal inflammation.
Insights
Follistatin neutralizes activins, promoting epithelial cell proliferation and tissue repair. This suggests follistatin as a potential treatment for intestinal inflammation and colitis in mice.
Area of Science:
- Gastroenterology
- Immunology
- Cell Biology
Background:
- Activins, part of the transforming growth factor-beta superfamily, are implicated in tissue repair and inflammation.
- Follistatin acts as a natural antagonist to activins.
- Previous research suggests a role for activins and follistatin in inflammatory processes.
Purpose of the Study:
- To investigate the in vivo anti-inflammatory effects of follistatin by neutralizing activins.
- To evaluate follistatin's efficacy in multiple murine models of colitis.
Main Methods:
- Assessed activin transcript levels in TNBS-induced colitis.
- Administered follistatin intraperitoneally before or after TNBS colitis induction.
- Examined established DSS-induced colitis and spontaneous colitis in IL-10 gene-deficient mice.
Main Results:
- Activin transcripts were upregulated in TNBS colitis; epithelial cells, macrophages, and endothelial cells produced excess activin betaA.
- Follistatin pretreatment increased survival in TNBS colitis (33% to 82%) and reduced IL-6 and amyloid A plasma levels.
- Follistatin reduced histologic scores and myeloperoxidase activity in TNBS and DSS colitis, and ameliorated colitis severity in IL-10-/- mice, promoting colonic epithelial cell proliferation.
Conclusions:
- Neutralization of activins with follistatin promotes epithelial cell division and enhances tissue repair.
- Follistatin demonstrates potential as a therapeutic strategy for managing intestinal inflammation.
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