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Published on: August 23, 2013
Rheumatoid blood decreases the adherence of polymorphonuclear cells (PMNs) to cultured endothelium
Abstract:
Rheumatoid sera and plasma inhibited the adherence of normal blood polymorphonuclear cells (PMNs) to cultured porcine endothelium. This inhibition of adhesion was not seen when PMNs were treated with the plasma or serum from normal subjects or patients with other inflammatory arthropathies. The abrogation of PMN adherence was directly related to the levels of circulating immune complexes and was not dependent upon the type of anti-inflammatory therapy that the patients were receiving nor on any of the recorded clinical parameters. A similar inhibition of adhesion was seen with heat induced aggregated human IgG (HAGG) provided that serum was present in the culture medium. In view of these results we propose that circulating immune complexes in RA may have a significant role in controlling the interaction of PMNs with vascular endothelium and in perpetuating the entry of these cells into the synovial fluid of the inflamed joints.
Insights
Rheumatoid arthritis patient sera and plasma block normal immune cell (polymorphonuclear cells, PMNs) adhesion to endothelium. This effect correlates with immune complex levels, suggesting a role in joint inflammation.
Area of Science:
- Immunology
- Rheumatology
- Cell Biology
Background:
- Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by joint swelling and pain.
- The precise mechanisms by which immune cells infiltrate joints in RA are not fully understood.
- Polymorphonuclear cells (PMNs) play a role in inflammatory processes.
Purpose of the Study:
- To investigate the effect of rheumatoid arthritis (RA) sera and plasma on polymorphonuclear cell (PMN) adherence to endothelium.
- To determine the relationship between PMN adherence inhibition and circulating immune complexes in RA patients.
Main Methods:
- Cultured porcine endothelium was used as a model system.
- Normal blood PMNs were incubated with sera or plasma from RA patients, healthy individuals, and patients with other inflammatory arthropathies.
- PMN adherence to the endothelium was measured.
- The effect of heat-aggregated human IgG (HAGG) on PMN adherence was also assessed in the presence of serum.
Main Results:
- Sera and plasma from RA patients significantly inhibited the adherence of normal PMNs to cultured endothelium.
- This inhibitory effect was specific to RA and not observed with samples from normal subjects or patients with other inflammatory arthropathies.
- The degree of PMN adherence inhibition correlated directly with the levels of circulating immune complexes in RA patients.
- The inhibition was independent of anti-inflammatory therapy and clinical parameters.
- Heat-aggregated human IgG (HAGG) mimicked this inhibitory effect in the presence of serum.
Conclusions:
- Circulating immune complexes in RA sera and plasma play a significant role in modulating the interaction between PMNs and vascular endothelium.
- These immune complexes may contribute to the perpetuation of PMN entry into the synovial fluid of inflamed joints in RA.
- Understanding this mechanism could offer new therapeutic targets for managing RA joint inflammation.
