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Modulation of kinin responses in human synovium by interleukin-1
J M Bathon1, J E Croghan, D W Goldman
1Johns Hopkins University School of Medicine, Department of Medicine, Baltimore, MD.
Agents and Actions. Supplements
|January 1, 1992
Summary
Interleukin-1 (IL-1) pretreatment makes human synovial cells more responsive to bradykinin (BK) by increasing prostaglandin E2 (PGE2) release. This involves more kinin receptors and enhanced calcium-dependent prostaglandin synthesis.
Area of Science:
- Inflammation research
- Cell signaling pathways
- Rheumatology
Background:
- Bradykinin (BK) is a vasoactive peptide involved in inflammatory processes.
- Prostaglandin E2 (PGE2) is a key mediator of inflammation and pain.
- Human synovial cells are implicated in joint inflammation.
Purpose of the Study:
- To investigate the effect of interleukin-1 (IL-1) on the responsiveness of human synovial cells to bradykinin (BK).
- To elucidate the mechanisms underlying IL-1-induced sensitization of synovial cells to BK for prostaglandin E2 (PGE2) release.
Main Methods:
- Human synovial cells were treated with IL-1.
- Cells were subsequently stimulated with BK.
- Prostaglandin E2 (PGE2) release was measured.
- Changes in kinin receptor expression and calcium-dependent signaling were assessed.
Main Results:
- Untreated synovial cells showed weak PGE2 release in response to BK.
- IL-1 pretreated cells exhibited a potent BK-induced PGE2 release.
- IL-1 upregulated kinin receptor numbers on synovial cells.
- IL-1 enhanced a calcium-dependent process in prostaglandin synthesis.
Conclusions:
- IL-1 significantly enhances BK-stimulated PGE2 release in human synovial cells.
- The mechanism is multifactorial, involving increased kinin receptors and augmented calcium-dependent prostaglandin synthesis.
- These findings provide insights into inflammatory signaling in synovial joints.