Functional changes of monocytes due to dialysis membranes

Abstract

The functional effects directly induced by dialysis membranes on peripheral monocytes were analyzed in a plasma-free model of simulated dialysis using Cuprophan, cuprammonium rayon, polyacrylonitrile, polymethylmetacrilate and polysulphone membranes. A severe reduction of monocyte phagocytosis of IgG-coated erythrocytes was found by using Cuprophan and cuproammonium rayon. The cytofluorimetric analysis of several cell surface receptors, involved in the immune phagocytosis and recognizable by five quoted monoclonal antibodies, did not reveal any significant change. The defective phagocytosis of the IgG-coated erythrocytes by monocytes, due to the exposure to cellulose-derived membranes, was paralleled by an impaired interiorization of heat-aggregated human immunoglobulins, as analyzed by electron microscopy. The cell membrane binding of aggregated immunoglobulins was found to be unaffected. The defect was associated to a remarkably depressed generation of reactive oxygen species after Zymosan stimulation. Therefore, the defective immune phagocytosis induced by exposure of monocytes to cellulosic membranes was not due to a receptor rearrangement or an impaired binding of ingestible particles, but to a reduced internalization capacity probably related to an energy source exhaustion (as shown by the lack of response to stimuli able to induce oxidizing species production). These features are similar to those described in monocytes from acute systemic lupus erythematosus patients.

Monocyte Activation in Peripheral Blood and Dialyser Eluates: Phenotypic Profile and Cytokine Release

“…These findings are interesting, as downregulation of HLA-DR on PBMC has been associated with a decreased capacity to present antigens [27]and a poor prognosis in both sepsis patients [28]and malnourished surgical patients [29]. With respect to the monocyte Fcγ receptor-I (CD64), it has been suggested that a functional defect is involved in the impaired phagocytosis of CHD patients [6, 7]. In our study, the expression of CD64 on PBMC was higher during HD with CU than PS devices, whereas DE was not different from PB.…”

“…In fact, most available data suggest an increased basal activation state, as estimated by changes in the expression of various cell surface markers and the release of pro-inflammatory cytokines. Remarkably, these signs of activation coincide with functional defects, such as reduced phagocytosis and impaired antigen presentation [6, 7]. …”

Oxidative Stress Potentials of Different Synthetic Hemodialysis Membranes

“…In patients receiving regular hemodialysis with cellulosic membranes, it has been shown that IL-1 and TNF-␣ levels, which were already high before the dialysis session because of complement activation, increased much more during the procedure. [1][2][3][4][5] It has been demonstrated that biocompatible synthetic membranes do not activate cytokine genes compared with cellulosic membranes. 6 Our results showed that PSU and EVAL, which are both synthetic membranes, do not cause signifi cant differences in proinfl ammatory cytokine release.…”

Clinical implications of biocompatibility in blood purification membranes

“…Recent studies have also indicated that monocytes have activation products such as thromboxane in mediating pulmonary hypertension. When sheep were pre-treated a receptor that can be activated directly by such membranes [14,28]. Therefore, a direct monowith cyclo-oxygenase inhibitors, the pulmonary effects of cellulosic-activated blood were abrogated [22,23].…”

“…Monocytes have specific activate Hageman factor (factor XII ) in vitro shows that PAN and cellulosic or cellulose-based membranes receptors for complement products and complement activation has been shown to result in increased tranactivate Hageman factor to a greater degree than do other membranes [7]. Furthermore, the differential scription of IL-1 and tumour necrosis factor-a ( TNF-a) [27,28]. Therefore, it is likely that some ability of dialysis membranes to activate Hageman factor-dependent pathways, as assessed by the forma-membranes such as cellulosic or cellulose-based membranes, which activate complement, may lead to tion of kallikrein and the subsequent generation of bradykinin, has also been shown [6,7].…”