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.

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 degrees 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 FcgammaR 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.

Severity of arthroscopically observed pathology and levels of inflammatory cytokines in the synovial fluid before and after visually guided temporomandibular joint irrigation correlated with the clinical outcome in patients with chronic closed lock.

OBJECTIVE: This study aimed to investigate the severity of arthroscopically observed pathologies and the levels of a set of inflammatory cytokines in aspirated synovial fluid (A-SF) in patients with chronic closed lock (CCL) of the temporomandibular joint (TMJ) before and after visually guided TMJ irrigation (VGIR). Furthermore, the findings were correlated with the clinical outcome after VGIR. STUDY DESIGN: VGIR was performed in 56 consecutive patients with unilateral CCL. Forty-nine of them, who underwent a second VGIR either as a follow-up arthroscopy or as a repeated therapeutic irrigation, were analyzed. They were assigned to either the successful (s-) group (n = 31) or unsuccessful (u-) group (n = 18), according to the clinical success criteria. The severity of arthroscopic findings of osteoarthritis (OA), synovitis, and fibrous adhesion (FA) were evaluated as arthroscopic scores. The levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, IL-8, IL-12, and IL-10 in the A-SF were measured. At the first and second VGIR, the arthroscopic scores and the levels of each investigated cytokine were compared between the s- and u-groups. In each group, same parameters were compared between the first and second VGIR. RESULTS: At the first and second VGIR, there are no differences in the arthroscopic scores between the s- and u-groups. After the first VGIR, the severity of synovitis significantly improved, that of OA was unchanged, and that of FA became worse in the s- and u-groups. At the first VGIR, the levels of IL-6 and IL-8 were significantly higher in the u-group, and the IL-10 level was significantly higher in the s-group. At the second VGIR, however, there were no differences in the levels of each investigated cytokine between the s- and u-groups. The levels of each cytokine did not significantly change between the first and second VGIR, regardless of the clinical outcome. CONCLUSIONS: VGIR may contribute to the remission of synovitis in patients with TMJ CCL. However, the severity of arthroscopically observed pathologies and the levels of each investigated cytokine do not seem to be reflected by the clinical state. Moreover even if the intra-articular inflammation is asymptomatic, an exacerbation may not be ruled out even after a successful VGIR.