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Angiogenesis blockade as a new therapeutic approach to experimental colitis

Silvio Danese1, Miquel Sans, David M Spencer

  • 1Division of Gastroenterology, Istituto Clinico Humanitas, Rozzano, Milan 20089, Italy. sdanese@hotmail.com

Gut
|December 16, 2006
PubMed
Abstract

Insights

Anti-angiogenic compound ATN-161 reduces inflammation and vascularity in experimental colitis models. This study suggests anti-angiogenic strategies may treat inflammatory bowel disease (IBD).

Area of Science:

  • Gastroenterology
  • Immunology
  • Vascular Biology

Background:

  • Neoangiogenesis is a key factor in chronic inflammatory disorders.
  • Anti-angiogenic therapies show promise in animal models of inflammation.
  • The efficacy of anti-angiogenesis in experimental colitis remained untested.

Purpose of the Study:

  • To evaluate the therapeutic potential of ATN-161, an anti-angiogenic agent, in experimental murine colitis.
  • To assess the impact of ATN-161 on angiogenesis and disease progression in colitis models.

Main Methods:

  • Interleukin 10-deficient (IL10(-/-)) and wild-type mice were used, some housed in ultra-barrier facilities (UBF).
  • Dextran sodium sulphate (DSS) induced acute colitis.
  • Mice received ATN-161 or a scrambled peptide (ATN-163); angiogenesis (CD31 staining, MVD), disease activity (DAI), histology, cytokine levels, and cell proliferation were assessed.

Main Results:

  • Vascular density (MVD) correlated with disease in conventional IL10(-/-) mice but not in UBF.
  • ATN-161 treatment significantly reduced disease activity index (DAI) and histological scores in IL10(-/-) mice with established colitis, accompanied by decreased MVD.
  • ATN-161 demonstrated no therapeutic effect in the DSS model or direct in vitro immunomodulatory activity.

Conclusions:

  • Active gut angiogenesis occurs in IL10(-/-) and DSS-induced colitis models, paralleling disease severity.
  • ATN-161 effectively reduced angiogenesis, clinical symptoms, and inflammation in IL10(-/-) mice, but not in DSS-treated mice.
  • These findings support the rationale for exploring anti-angiogenic therapies for human inflammatory bowel disease (IBD).

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