Increased synovial galectin-3 induce inflammatory fibroblast activation and osteoclastogenesis in patients with rheumatoid arthritis
Authors' conclusion
An initial decrease in plasma Gal-3 levels predicted decreased long-term disease activity. Correspondingly, a Gal-3 inhibitor decreased the activity of inflammatory FLSs and osteoclastogenesis in patients with RA.
Study context
- Population
- Healthy controls and patients with newly diagnosed early rheumatoid arthritis (RA) or chronic RA
- Comparison
- RA vs healthy controls; Gal-3 inhibitor vs controls in vitro
- Healthy controlsn = 48reference
- Chronic RAn = 18
- Outcome
- Gal-3 in RA
Methodological detailscase-control plasma comparison, in vitro FLS monocultures and autologous FLS/PBMC co-cultures
- Case-control plasma comparison
- In vitro FLS monocultures and autologous FLS/PBMC co-cultures
Main finding
As reported in the abstract
- Seropositive early RA: all patients with decreasing plasma Gal-3 from 0 to 3 months had low disease activity after 2 years
- p < 0.05
- Gal-3 inhibitor (GB1107, 10 µM) significantly reduced IL-1β and TNF-α secretion from FLS monocultures
- both p < 0.05
- Gal-3 inhibitor decreased monocyte-derived osteoclastogenesis vs controls
- both p < 0.05
Original publication
Increased synovial galectin-3 induce inflammatory fibroblast activation and osteoclastogenesis in patients with rheumatoid arthritis. Scand J Rheumatol. Published 13 January 2022. doi:10.
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