Title: Matrix metalloproteinase-9 deficiency impairs host defense against abdominal sepsis
Authors: Renckens, Rosemarijn ×
Roelofs, Joris J. T. H
Florquin, Sandrine
de Vos, Alex F
Lijnen, Roger
van't Veer, Cornelis
van der Poll, Tom #
Issue Date: Mar-2006
Publisher: American Association of Immunologists
Series Title: Journal of Immunology vol:176 issue:6 pages:3735-3741
Conference: date:Univ Amsterdam, Acad Med Ctr, Lab Expt Internal Med, NL-1105 AZ Amsterdam, Netherlands; Univ Amsterdam, Acad Med Ctr, Dept Pathol, NL-1105 AZ Amsterdam, Netherlands; Univ Amsterdam, Acad Med Ctr, Dept Infect Dis Trop Med & AIDS, NL-1105 AZ Amsterdam, Netherlands; Katholieke Univ Leuven, Ctr Mol & Vasc Biol, Louvain, Belgium
Abstract: Matrix metalloproteinase (MMP)-9 is involved in extracellular matrix degradation and leukocyte migration. To determine the role of MMP-9 in the innate immune response to peritonitis, MMP-9 gene-deficient (MMP-9(-/-)) and normal wild-type mice were i.p. infected with Escherichia coli. MMP-9 mRNA and pro-MMP-9 protein levels increased rapidly upon induction of peritonitis. Although MMP-9(-/-) neutrophils showed a normal phagocytosis of E. coli in vitro, MMP-9(-/-) mice displayed a reduced resistance against E. coli peritonitis, as indicated by an enhanced bacterial outgrowth in the peritoneal cavity and increased dissemination of the infection. Furthermore, the cytokine response to LPS was not influenced by MMP-9 deficiency. However, during E. coli peritonitis, MMP-9(-/-) mice showed much higher peritoneal chemokine and cytokine levels compared with wild-type mice. Despite the increased local chemokine concentrations, MMP-9(-/-) mice displayed a diminished recruitment of leukocytes to the site of infection, indicating that cellular migration was impaired. Moreover, MMP-9(-/-) mice developed more severe distant organ damage during infection. These data suggest that MMP-9 is an essential component of an effective host response to E. coli peritonitis.
ISSN: 0022-1767
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Molecular and Vascular Biology
× corresponding author
# (joint) last author

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