Studies on the Mechanisms of Leukocyte Adhesion to Cellulose Acetate Beads: An In Vitro Model to Assess the Efficacy of Cellulose Acetate Carrier-based Granulocyte and Monocyte Adsorptive Apheresis
Article first published online: 24 JUN 2003
Therapeutic Apheresis and Dialysis
Volume 7, Issue 3, pages 334–340, June 2003
How to Cite
Hiraishi, K., Takeda, Y., Shiobara, N., Shibusawa, H., Jimma, F., Kashiwagi, N., Saniabadi, A. R. and Adachi, M. (2003), Studies on the Mechanisms of Leukocyte Adhesion to Cellulose Acetate Beads: An In Vitro Model to Assess the Efficacy of Cellulose Acetate Carrier-based Granulocyte and Monocyte Adsorptive Apheresis. Therapeutic Apheresis and Dialysis, 7: 334–340. doi: 10.1046/j.1526-0968.2003.00049.x
- Issue published online: 24 JUN 2003
- Article first published online: 24 JUN 2003
- Received February 2003.
- Adsorptive apheresis;
- Cellulose acetate;
- Granulocytes and monocytes;
- TNF receptors
Abstract: Granulocyte and monocyte adsorptive apheresis (GMA) using a column filled with cellulose acetate (CA) beads (carriers) has been associated with a significant clinical efficacy in patients with rheumatoid arthritis and ulcerative colitis. To obtain further understanding on the mechanisms of disease modification by cellulose acetate-carrier-based GMA, in the present study, we investigated the mechanisms of granulocyte and monocyte adhesion to CA beads following exposure of human peripheral blood to the carriers at 37°C for up to 60 min under controlled conditions. Cellulose acetate beads selectively adsorbed granulocytes, monocytes, CD19+ (B cells) and CD56+ (NK cells) lymphocyte subpopulations. The granulocyte and monocyte adsorption was inhibited by heat-inactivated plasma and EDTA, indicating that the adsorption was plasma protein (immunoglobulin, complement) and calcium dependent. Accordingly, granulocyte and monocyte adsorption was markedly enhanced by coating the carriers with IgG. Similarly, C3b was adsorbed onto the CA beads as a marker of complement activation. The results indicated that IgG and active complement fragments mediated leukocyte adhesion to CA beads via the FcγR and/or leukocyte complement receptor like CR3. Additionally, CA beads induced loss of expression of TNF receptors on CD16+ granulocytes and CD14+ monocytes, but not on CD3+ lymphocytes. In conclusion, CA beads might be an appropriate biomaterial for inducing extracorporeal immunomodulation as a treatment for auto-immune diseases which are associated with pathological leukocyte activity.