Inhibition of gelatinase B/MMP-9 does not attenuate colitis in murine models of inflammatory bowel disease

Magali de Bruyn, Christine Breynaert, Ingrid Arijs, Gert De Hertogh, Karel Geboes, Greet Thijs, Gianluca Matteoli, Jialiang Hu, Jo Van Damme, Bernd Arnold, Marc Ferrante, Séverine Vermeire, Gert Van Assche and Ghislain Opdenakker ()
Additional contact information
Magali de Bruyn: Laboratory of Immunobiology, Rega Institute for Medical Research, KU Leuven
Christine Breynaert: Laboratory of Clinical Immunology, KU Leuven
Ingrid Arijs: Translational Research Center for Gastrointestinal Disorders (TARGID), KU Leuven
Gert De Hertogh: Translational Cell and Tissue Research, KU Leuven
Karel Geboes: Translational Cell and Tissue Research, KU Leuven
Greet Thijs: Laboratory of Immunobiology, Rega Institute for Medical Research, KU Leuven
Gianluca Matteoli: Translational Research Center for Gastrointestinal Disorders (TARGID), KU Leuven
Jialiang Hu: Key Laboratory of Modern Chinese Medicines, Ministry of Education, China Pharmaceutical University
Jo Van Damme: Laboratory of Molecular Immunology, Rega Institute for Medical Research, KU Leuven
Bernd Arnold: German Cancer Research Center (DKFZ)
Marc Ferrante: Translational Research Center for Gastrointestinal Disorders (TARGID), KU Leuven
Séverine Vermeire: Translational Research Center for Gastrointestinal Disorders (TARGID), KU Leuven
Gert Van Assche: Translational Research Center for Gastrointestinal Disorders (TARGID), KU Leuven
Ghislain Opdenakker: Laboratory of Immunobiology, Rega Institute for Medical Research, KU Leuven

Nature Communications, 2017, vol. 8, issue 1, 1-15

Abstract: Abstract One third of patients with inflammatory bowel disease (IBD) inadequately respond to anti-TNF treatment and preclinical data suggest that matrix metalloproteinase-9 (MMP-9) is a novel therapeutic target. Here we show that IBD clinical and histopathological parameters found in wild type mice challenged with three different models of colitis, acute and chronic dextran sodium sulphate (DSS), and acute 2,4,6-trinitrobenzenesulfonic acid-induced colitis are not attenuated in MMP-9 knockout mice. We find similar colonic gene expression profiles in wild type and MMP-9 knockout mice in control and acute DSS conditions with the exception of eleven genes involved in antimicrobial response during colitis. Parameters of chronic colitis are similar in wild type and MMP-9 knockout mice. Pharmacological inhibition of MMP-9 with bio-active peptides does not improve DSS colitis. We suggest that MMP-9 upregulation is a consequence rather than a cause of intestinal inflammation and we question whether MMP-9 represents a disease target in IBD.

Date: 2017
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DOI: 10.1038/ncomms15384

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