ArticleRheumatology international2006
Expression of ICAM-1, ICAM-2, NCAM-1 and VCAM-1 by human synovial cells exposed to Borrelia burgdorferi in vitro.
Article in Rheumatology international, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 4 citations in OpenAlex.
- Lyme arthritis: current concepts and a change in paradigm.Clinical and vaccine immunology : CVI · 2008Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The interaction of resident tissue cells with migratory inflammatory cells is essential for the recruitment of immune effector cells to inflammatory sites. The sustained expression of adhesion molecules in the synovium of patients with chronic Lyme arthritis seems to contribute to this chronic inflammation. Whether cell adhesion molecules influence the early steps of Borreliosis is unclear. Therefore, we examined the expression of ICAM-1, ICAM-2, VCAM-1 and NCAM-1 in synovial cells exposed to two different Borrelia burgdorferi sensu stricto strains Geho and B31. The mRNA expression of ICAM-1, ICAM-2, VCAM-1 and NCAM-1 was not changed in synovial cells exposed to B31. Whereas ICAM-2 and VCAM-1 was upregulated, NCAM-1 mRNA was downregulated and ICAM-1 mRNA was unchanged by strain Geho. The ICAM-1 protein expression on the synovial cell surface was downregulated by both strains. Differential regulation of adhesion molecule mRNA, and subsequent high turnover or elevated shedding from the cell membrane may contribute to early pathogenesis in Lyme arthritis.
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Registered trials
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