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Published online before print May 9, 2006

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(Journal of Leukocyte Biology. 2006;80:125-132.)
© 2006 by Society for Leukocyte Biology

Enhanced early vascular permeability in gelatinase B (MMP-9)-deficient mice: putative contribution of COX-1-derived PGE₂ of macrophage origin

Elzbieta Kolaczkowska^*,1, Anna Scislowska-Czarnecka^*,, Magdalena Chadzinska^*, Barbara Plytycz^*, Nico van Rooijen, Ghislain Opdenakker and Bernd Arnold^¶

^* Department of Evolutionary Immunobiology, Institute of Zoology, Jagiellonian University Krakow, Poland;
Department of Physiotherapy, Faculty of Anatomy, Academy of Physical Education, Krakow, Poland;
Department of Molecular Cell Biology, Faculty of Medicine, Vrije Universiteit, Amsterdam, The Netherlands;
Laboratory of Immunobiology, Rega Institute for Medical Research, University of Leuven, Belgium; and
^¶ Laboratory for Molecular Immunology, German Cancer Research Center, Heidelberg, Germany

¹ Correspondence: Department of Evolutionary Immunobiology, Institute of Zoology, Jagiellonian University, ul. Ingardena 6, PL-30-060 Krakow, Poland. E-mail: kolac{at}zuk.iz.uj.edu.pl

Increased vascular permeability leading to vascular leakage is a central feature of all inflammatory reactions and is critical for the formation of an inflammatory exudate. The leakage occurs because of gap formation between endothelial cells and breakdown of the basement membrane barriers. The present study aimed to investigate the role of gelatinase B [matrix metalloproteinase 9 (MMP-9)], known to be involved in neutrophil exudation, in changes of vascular permeability at the early stages of acute zymosan peritonitis. We show that although MMP-9 is being released already within the first minutes of peritonitis, its lack, induced pharmacologically or genetically, does not decrease but rather increases vasopermeability. In mice treated with an inhibitor of gelatinases (A and B), a tendency to increased vasopermeability existed, and in MMP-9–/– mice [knockout (KO)], the difference was statistically significant in comparison with their controls. Moreover, in intact KO mice, significantly augmented production of prostaglandin E₂ (PGE₂) of cyclooxygenase 1 (COX-1) origin was detected, and depletion of peritoneal macrophages, but not mast cells, decreased vasopermeability in KO mice. Thus, the increase of vasopermeability observed on KO mice is a result of the increased production of COX-1-derived PGE₂ by peritoneal macrophages. We conclude that genetic deficiency in gelatinase B might lead to the development of a compensatory mechanism involving the COX pathway.

Key Words: metalloproteinase-9 • peritonitis • peritoneal inflammation • vasopermeability • cyclooxygenase • prostaglandin

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