학술논문

Matrix metalloproteinase-9 (gelatinase B) deficiency leads to increased severity of Staphylococcus aureus-triggered septic arthritis
Document Type
Report
Source
Microbes and Infection. May, 2006, Vol. 8 Issue 6, p1434, 6 p.
Subject
Rheumatoid factor -- Analysis
Rheumatoid arthritis -- Analysis
Arthritis, Infectious -- Analysis
Infectious arthritis -- Analysis
Language
English
ISSN
1286-4579
Abstract
To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.micinf.2006.01.001 Byline: Ann-Marie Calander (a), Sofie Starckx (b), Ghislain Opdenakker (b), Philip Bergin (c), Marianne Quiding-Jarbrink (c), Andrej Tarkowski (a) Abstract: Matrix metalloproteinases constitute a family of structurally related endopeptidases that are crucial for the normal turnover of the extracellular matrix. Elevated levels of MMP-9 have been demonstrated in synovial fluids of rheumatoid arthritis patients, and a correlation with the severity of the disease has been described. The aim of this study was to explore the impact of MMP-9 expression on joint inflammation and destruction in a model of bacterially induced septic arthritis. MMP-9 knock-out mice and C57Bl6 congenic controls were inoculated intravenously or intra-articularly with Staphylococcus aureus. Arthritis was evaluated clinically and by means of histology. Zymographic analyses were performed to study ex vivo induction of MMP-9 following exposure to S. aureus. The MMP-9 knock-out mice displayed a significantly higher frequency and severity, but not destructivity, of arthritis than did the wild-type mice. The knock-out mice also proved to harbour an increased number of bacteria locally in joints and systemically in kidneys, possibly by impaired extravasation and recruitment of leukocytes and a deficient early defence against infection. Our findings indicate that deficiency in MMP-9 increases the degree of joint inflammation due to decreased bacterial clearance. Author Affiliation: (a) Department of Rheumatology and Inflammation Research, University of Gothenburg, Guldhedsgatan 10A, S-413 46 Gothenburg, Sweden (b) Rega Institute for Medical Research, University of Leuven, Minderbroedersstraat 10, Leuven, Belgium (c) Department of Medical Microbiology and Immunology, University of Gothenburg, S-405 30 Gothenburg, Sweden Article History: Received 15 December 2005; Accepted 3 January 2006