Differential expression of matrix metalloproteinases and cyclooxygenases in synovial cells exposed to Borrelia burgdorferi
Abstract
OBJECTIVE AND DESIGN: Lyme arthritis is characterized by strong inflammatory reactions probably due to the presence of Borrelia burgdorferi in the joint. It has been suggested that Borrelia adopts different molecular mechanisms that either can amplify the host's inflammatory response or can suppress it. In the present study we analyzed the induction of matrix metalloproteinases (MMPs) and cyclooxygenases (COXs) in human synoviocytes exposed to different B. burgdorferi sensu stricto isolates (Geho and B31). MATERIALS AND METHODS: Synoviocytes were exposed in vitro for 12 h up to 5 days. Semiquantitative reverse transcription polymerase chain reaction was used to assess the mRNA expression of MMP-1 to 13, COX-1 and COX-2. Prostaglandin E2 (PGE2) production was assessed by ELISA. RESULTS: MMP-1 was unchanged in synovial cells exposed to strain Geho, whereas it was downregulated by strain B31. MMP-13 was downregulated by both strains. COX-2 was upregulated by strain B31, which resulted in increased PGE2 concentration in the supernatant. In contrast, COX-1 was slightly upregulated and COX-2 tended to be downregulated by Geho resulting in a decreased PGE2 concentration. CONCLUSIONS: The differential expression of MMPs and COXs suggests that different B. burgdorferi strains influence different molecular mechanisms leading to chronic inflammation. This might be reflected in the clinical variability among Lyme arthritis patients.
Key Biomarkers
Symptom Clusters
References (3)
- Lipoproteins of Borrelia burgdorferi and Treponema pallidum activate cachectin/tumor necrosis factor synthesis. Analysis using a CAT reporter constructThe Journal of Immunology · 1991
- Fibroblasts protect the Lyme disease spirochete, Borrelia burgdorferi, from ceftriaxone in vitroThe Journal of Infectious Diseases · 1992
- Ultrastructural demonstration of spirochetal antigens in synovial fluid and synovial membrane in chronic lyme disease: Possible factors contributing to persistence of organismsHuman Pathology · 1996
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