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Control of immune complex and zymosan-mediated anaphylatoxin generation by proteins B and H of the alternative complement pathway.

The generation of histamine releasing activity (HRA) from human basophils in fresh serum by tetanus toxoid (Te)/anti-Te complexes or by zymosan can be modulated through introduction of incremental amounts of proteins B and H of the alternative complement pathway. Serum treated at 50 degrees in order to abolish alternative pathway-mediated haemolytic activity, lost 90% of its capacity to generate HRA upon addition of Te/aTe; such loss could be reversed through additions of purified B. Amounts of B sufficient to restore normal alternative pathway haemolytic activity also restored HRA induced by Te/aTe; as little as a 33% increase above the normal serum concentration of B increased the capacity to support Te/aTe induced HRA by a factor of 1.4. In contrast, additions of incremental doses of purified H to fresh serum reduced generation of HRA by both Te/aTe and zymosan. Total inhibition was achieved by increasing the serum H concentration by 12.5-30%; further increases of H up to 200% again permitted HRA generation induced by immune complexed aTe. H also inhibited Te/aTe induced HRA in a serum heated at 50 degrees but only 30% inhibition of HRA could be achieved over a range of H inputs up to 187% above normal serum concentration. Additions of H also inhibited HRA generation in fresh serum when induced with plain or C3b-coated zymosan (Z) particles. By increasing the serum concentration of H from 12.5 to 125%, dose-dependent inhibition of HRA generation was observed; the H input necessary to suppress 48% of HRA generation was ten times higher when HRA was generated by Z-C3b than by plain zymosan. Thus, the complement-dependent generation of HRA from fresh serum strongly depends on modest variations in the concentrations of the two regulatory proteins B and H of the alternative complement pathway, suggesting their direct effect on generation of anaphylatoxins C3a and C5a.

Anaphylatoxins↗

Blood platelets activate the classical pathway of human complement.

OBJECTIVE: Activation of the complement system plays a key role in inflammation associated with vascular injury. Recently, platelet P-selectin was shown to activate C3 via the alternative pathway of human complement. As platelets also posses binding sites for C1q, the recognition unit of the classical complement pathway, the present study examined classical pathway activation on platelets. METHODS: Complement activation was assessed by either a solid phase enzyme-linked immunosorbent assay (ELISA) or flow cytometry. RESULTS: Using the ELISA approach, 2- to 10-fold increases (P < 0.001) in C1q and C4d deposition were demonstrated on adherent platelets following exposure (60 min 37 degrees C) to diluted (1/10) human plasma or serum. Similar results were obtained by flow cytometry using activated platelets in suspension. C1q and C4d deposition on platelets was accompanied by an approximately 4-fold increase in fluid phase C4d and C3a generation. Consistent with activation of the classical complement pathway, C4 cleavage failed to occur in serum depleted of C1q but was unchanged in factor B deficient serum. C4 activation was enhanced by platelet stimulation using chemical (SFLLRN peptide) or mechanical (shear) means, and decreased following platelet exposure to plasmin. These treatments were accompanied by changes in platelet surface gC1qR/p33 expression, a cellular C1q binding protein. In purified systems, recombinant gC1qR/p33 supported C4 activation, in a C1q dependent manner. CONCLUSION: These data provide the first evidence for C1q dependent classical complement pathway activation on platelets, and support a role for gC1qR/p33 in this process. However, monoclonal antibodies (mAb) to gC1qR/p33 produced only modest (20% +/- 8%, mean +/- SD, n = 5) reductions in C4 activation on platelets. Thus, further studies are required to investigate the involvement of additional platelet membrane constituents in classical complement pathway activation.

Blood Platelets↗

Storage of buffy coat preparations at 22 degrees C in plastic containers with different gas permeability.

BACKGROUND: Buffy coats (BCs) are used as an alternative to platelet-rich plasma in the preparation of platelet concentrates (PCs). For this purpose the BCs have to be stored for same time at 20-24 degrees C which implies cellular metabolic activity. However, little information is available concerning the effects of a number of factors which may influence the suitability of the preparation as the source of PC. STUDY DESIGN AND METHODS: We studied the effects on BCs of a high and low gas permeability of the wall of the plastic containers, PL2209 and PL146, respectively, mixing versus non-mixing during storage for 48 h at 22 degrees C, and two types of anticoagulant solutions, CPD and half strength citrate CPD (0.5CPD). The buffy coats were prepared by the bottom and top technique. The median values of volume and haematrocrit were 58-64 ml and 39-45%, respectively. A total of 48 BCs were tested. Blood gases, pH, bicarbonate concentration and haemolysis were determined in the blood mixtures and beta-thromboglobulin (beta-TG), lactate dehydrogenase (LDH), complement factor 3a, and elastase in the extracellular fluid. RESULTS: The pH decreased in all units but to a lesser extent in PL2209 containers than in PL146 units. In the former the pCO2 decreased slowly in contrast to the latter where it increased by about 50%. Mixing during storage increased the pH and decreased the pCO2 in 0.5CPD-PL146 and CPD-PL2209 units, as compared to resting, while no effects of mixing were observed in the other groups. The pO2 decreased to low levels in PL146 units. The haemolysis and LDH release were higher in mixed than in unmixed units. The initial beta-TG levels were lowest in 0.5CPD-PL146 units which also had the lowest 24-hour levels. The release of beta-TG during storage was smallest in CPD resting units. The elastase release was significantly higher in 0.5CPD than in CPD units already from the beginning of storage and increased during storage at about the same rate irrespective of mixing. The C3a levels were higher in 0.5CPD-PL2209 units than in the other units at 2 h. Storage for 24 h caused an increase by 2-3 times of the original level without any clear relation to storage conditions. CONCLUSIONS: In BC units accumulation of CO2 occurs in containers with low gas permeability. These also show the most rapid pH decrease during storage. Prolonged holding of BCs puts extra emphasis on the need of satisfactory gas permeability of the container for platelet storage in BC-derived PCs. Continuous mixing causes red cell damage and does not seem to have any clear benefit. The release of granulocyte elastase was higher in 0.5CPD than in CPD units but there was no indication of an associated increase in platelet activation. SUMMARY: Study of buffy coats stored in various media and containers at 22 degrees C suggests that it is better to restrict storage to 24 h or less to avoid activation or other deleterious effects on the platelets.

Blood Gas Analysis↗

Frequent expression of complement resistance factors CD46, CD55, and CD59 on gastrointestinal cancer cells limits the therapeutic potential of monoclonal antibody 17-1A.

BACKGROUND: One reason for the failure of monoclonal antibody (mab) trials in most cancer patients might be the presence of complement resistance factors that inhibit complement dependent cytotoxicity (CDC) and the release of inflammatory mediators (e.g., anaphylatoxins). METHOD: We have determined the expression of CD46, CD55, and CD59 in five gastric, three colon, and seven pancreatic human cancer cell lines by immunostaining. The complement activating properties of mabs and conjugates with cobra venom factor (CVF) were studied in a 51Cr-release toxicity assay and in an ELISA to determine the release of C3a. RESULT: Virtually all tumor cell lines strongly expressed CD46, CD55, and CD59, except KATOIII gastric cancer cells (CD55 and CD59 negative). In accordance with other studies we could confirm that expression of CD55 and CD59 inhibits a complement activation by mabs. Whereas 17-1A was able to induce a cytotoxic complement activation on KATOIII cells, neither a CDC nor an anaphylatoxin release (C3a) was observed on MKN28 cells (strong expression of CD55 and CD59). Conjugation with CVF, a strong activator of the alternative pathway of complement, could partially restore the complement activation by mabs. A 17-1A-CVF conjugate, although still nontoxic, induced the release of the anaphylatoxin C3a on both cell lines. The same observations were made in PancTuI pancreatic cancer cells treated with a conjugate of the mab CA19-9 and CVF. CONCLUSIONS: Our study shows that complement resistance is a frequent event in gastrointestinal cancer, limiting the potential of monoclonal antibodies. Mabs, when conjugated with CVF, partially retain complement activating properties by releasing C3a, which in vivo will support a cellular immune response.

Antibodies, Monoclonal↗

Ixodes dammini: salivary anti-complement activity.

Saliva of the tick Ixodes dammini prevents hemolysis of rabbit erythrocytes by the human alternative pathway of complement. Deposition of C3b to activating surfaces and concomitant C3a release are inhibited. C3b deposition to activating surfaces is inhibited regardless the origin (humans, rat, mouse, guinea pig, and hamster) of the serum. The inhibitor elutes as a single peak upon gel filtration, with an apparent molecular weight of 49,000. Salivary anti-complement may contribute to successful feeding of I. dammini in their natural hosts.

Animals↗

Clonal variations in complement activation and deposition of C3b and C4b on model immune complexes.

This study examined the relationship between complement activation and the deposition of C3b and C4b on a panel of model immune complexes (IC). IC were constructed by combining murine monoclonal IgM, IgA, IgG1, IgG2a or IgG3 anti-dinitrophenyl (DNP) antibodies with DNP-bovine serum albumin (DNP-BSA). The IC were incubated with human plasma as a complement source and the formation of C4a and C3a, as well as the deposition of C4b and C3b on the IC, measured by radioimmunoassay. The results indicate that there were isotype-independent variations in the capacity of different types of IC to activate the classical pathway, especially for isotype-matched pairs of IC containing IgG1, IgG2a and IgG3 antibodies. In most cases, there was a direct relationship between classical pathway activation and the cleavage of C3. There was, for most of the IC, a direct correlation between cleavage of C4 and C3 and the subsequent deposition of C4b and C3b on the IC. However, a pair of IC constructed with independently derived IgG1 antibodies was virtually identical with respect to C3 cleavage and yet differed in the number of C3b molecules deposited on the IC. Collectively, these data suggest that the immunoglobulin variable region can play a significant role in both complement activation and the deposition of C3b and C4b on IC.

Antigen-Antibody Complex↗

The possible role of Limulus-amebocyte-lysate-reactive material in hemodialysis. First-use syndrome.

Hypersensitivity-like reactions are an infrequent but persistent clinical manifestation of hemodialysis. Although a Limulus-amebocyte-lysate-reactive material (LAL-RM) has been demonstrated in some hemodialyzers, its potential role in causing anaphylactoid reactions has not been addressed heretofore. In this chapter, current knowledge about LAL-RM will be presented and integrated with the major mechanisms generally recognized to induce hypersensitivity-type reactions. These mechanisms include: classical induction of allergy by IgE and classical complement activation by IgG and IgM. Alternative complement activation will be not discussed as it has been extensively reported in the literature of hemodialysis and because LAL-RM has not been shown to activate C3a extensively.

Anaphylaxis↗

A monoclonal antibody-cobra venom factor conjugate increases the tumor-specific uptake of a 99mTc-labeled anti-carcinoembryonic antigen antibody by a two-step approach.

Monoclonal antibodies (mabs) have considerable potential for specific cancer treatment. However, due to the antigen heterogeneity and especially the low uptake in solid tumors, mabs have not been used successfully in most clinical trials to date. This study investigates the effects of a mab-cobra venom factor (CVF) conjugate in vitro and in vivo in an orthotopic pancreatic cancer model using nude rats. CVF, a nontoxic glycoprotein from cobra venom, permanently activates the alternative pathway of complement. Coupled to a mab with tumor-binding properties, the complement activation can be targeted to the tumor tissue. We studied the activity of a mab CA19-9-CVF conjugate with the human pancreatic cancer cells PancTu I. PancTu I cells express the complement resistance factors CD46, CD55, and CD59, as we demonstrated by immunostaining, an observation that may explain the lack of cytotoxicity of the CA19-9-CVF conjugate. However, using ELISA, Western blot, and immunostaining, we showed that CA19-9-CVF activates the complement cascade, including the release of the anaphylatoxin C3a, a mediator of an inflammatory reaction. The in vivo studies of CA19-9-CVF-treated nude rats showed an increased tumor infiltration by natural killer cells and macrophages. The tumor uptake of 99Tc-labeled anti-carcinoembryonic antigen antibody was increased approximately 2-fold in rats pretreated with 70 micrograms of CA19-9-CVF, compared to animals that received an equimolar mixture of noncoupled mab and CVF. This study indicates the value of mab-CVF conjugates in adjuvant immunotherapy. mab-CVF conjugates might be useful in pretargeting approaches by increasing the uptake of a therapeutic mab.

Animals↗

Evaluation of complement activation in premature newborn infants with hyaline membrane disease.

Fifteen premature newborns with hyaline membrane disease causing acute respiratory distress were evaluated for complement activation. A high intrapulmonary right-to-left shunt and marked arterial-alveolar oxygen difference indicated the severity of the respiratory failure. Twenty preterm healthy infants served as controls. Total haemolytic activity, plasma concentrations of complement components and regulatory proteins (C3, C4, C1-inhibitor, factors H and I) as well as activation products (C3a, C3dg, C1rsC1-inhibitor, C3b(Bb)P) gave no evidence of significant complement activation. Functional activity of the ubiquitous regulatory protein C1-inhibitor was significantly reduced without impact on classical pathway activation. These data suggest that, in contrast to the adult form of respiratory distress syndrome, the low-pressure pulmonary oedema characterising hyaline membrane disease is not mediated by activation of the complement system.

Biomarkers↗

Possible role of free radical altered IgG in the etiopathogenesis of rheumatoid arthritis.

Alteration of IgG by oxygen-derived free radicals has been implicated in an in vivo process which renders IgG autoantigenic and leads to the production of rheumatoid factor (RF) and the perpetuation of inflammation, as in rheumatoid arthritis (RA). In this study the impact of UV irradiation on IgG was investigated as well as the ability of RF to bind to UV-altered gamma globulin. Inhibition studies of the binding of 125I aggregated human gamma globulin (AHG) to RF-coated sepharose beads show that UV-irradiated IgG is able to bind RF to the same extent as AHG. Binding studies to 125I-C1q proved that UV-irradiated IgG could bind the first complement component, but also that the complement system could be activated as illustrated by the C3a generation. These results support the hypothesis that free radical damage to gamma globulins plays a role in the chronicity of the inflammatory reaction in RA.

Arthritis, Rheumatoid↗

The effect of antibody isotype on the activation of C3 and C4 by immune complexes formed in the presence of serum: correlation with the prevention of immune precipitation.

Radioimmunoassays for C3a and C4a have been used to measure the activation of complement during the formation of immune complexes in human serum by the interaction of DNP-BSA and each of 11 mouse anti-DNP monoclonal antibodies of varied isotype and affinity. Those containing IgG2 or IgM were potent activators of C4, whilst IgG1 containing complexes were less efficient. C3 activation in normal serum was similar for complexes containing IgG1, IgG2a, IgG2b or IgM. IgA complexes did not activate C3 or C4. All complexes except those containing IgA precipitated more slowly in serum than in buffer. IgG2 antibodies were potent activators despite being very slow to precipitate in buffer. In serum containing EGTA activation of C4 was abolished and precipitation of complexes occurred at the same rate as in buffer. Nevertheless, C3 activation still occurred by the alternative pathway for all IgG and IgM complexes. Antibodies of the same isotype did not necessarily activate complement to the same extent. The ranking of the ability to activate complement was the same as that observed when performed complexes containing the same antibodies were added to serum. The levels of C4a generated were similar under both conditions but for most antibodies more C3a was generated by preformed complexes.

Antibodies, Monoclonal↗

Fluid phase generation of terminal complement complex as a novel index of bioincompatibility.

Blood membrane interactions in hemodialysis have been shown to trigger complement (C) activation. As indicators of C-activation the anaphylatoxins (C3a and C5a) are problematical because of methodological difficulties and their kinetic properties. We developed a sensitive and specific micro-ELISA using a monoclonal antibody against neoantigens on the terminal complement complex (TCC); highly purified human TCC served as standard. Concentrations of TCC were measured in single-path perfusion systems (in vitro) and in the blood lines (arterial inlet; venous outlet) of patients on hemodialysis using steam-sterilized or ETO-sterilized dialyzers with the following membranes: cuprophan (CU), hemophan (HE) and polysulfone F6 (PS), respectively. All dialyzers with identical geometry were run under identical conditions. All membranes tested caused continuously ongoing net generation of TCC. In vitro, contact of serum with CU minidialyzers resulted in fivefold higher net release of TCC compared with HE and PS. In vivo TCC concentration-time profiles differed significantly between membranes in the rank order CU much much greater than HE greater than PS (mean basal concentration 58 x 10(-11) M; peak increase over baseline with CU 40-fold, HE fourfold, PS threefold). In addition, more TCC was generated from the same dialyzers with ETO than steam sterilization. TCC differed from C3a and C5a in the following respects: (i) lower detection limit (4 x 10(-11) vs. less than 5 x 10(-9) M for both C-anaphylatoxins); (ii) higher relative increment (inlet) during CU dialysis (25-fold vs. eightfold and twofold, respectively); (iii) C-anaphylatoxins yielded the same ranking (CU much greater than HE greater than PS), but TCC concentrations were not a linear function of C3a or C5a concentrations, respectively. Kinetic analysis (Bateman function) showed significant differences of invasion constants between membranes, that is, CU 0.088 min-1, HE 0.09, PS 0.168. The net amount of TCC released from the dialyzer was calculated under certain assumptions. It was 75.5 mg/4 hr for CU, 7.3 for HE and 5.0 for PS. The elimination constant was also dependent on the type of membrane. Using flow cytofluorometry and immunohistochemical methods (APAAP), TCC was demonstrated on membranes of granulocytes obtained during dialysis; this is compatible with potential in vivo cell activation. Generation of PGE2 and TNF alpha by adherent monocytes induced by cuprophan was C8 dependent: levels were significantly increased by addition of C8 to C8 deficient human serum concomitantly with generation of TCC.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Purification and partial characterization of human and porcine C3a anaphylatoxin.

C3a anaphylatoxin is a protein fragment generated enzymatically in serum during activation of the third component of complement (C3). A four-step procedure is described for the purification of human and porcine C3a anaphylatoxins from their respective sera after activation with inulin. Because serum carboxypeptidase rapidly inactivates C3a, the inhibitor epsilon-aminocaproic acid (EACA) was added during C3 activation, thus permitting isolation of fully active C3a anaphylatoxins directly from serum. A 2000-fold purification of C3a was achieved with an average 30% recovery assuming total conversion of C3 during treatment of serum with inulin. Human C3a anaphylatoxin obtained through the action of the C3 activating enzyme of the "alternate" pathway appeared nearly identical with the C3a obtained from isolated C3 after treatment with the C4,2 enzyme of the "classical" pathway or with trypsin. Comparisons were made between various properties of human and porcine C3a anaphylatoxins. The molecular weights differed only slightly. Electrophoresis on a cellulose acetate strip at pH 8.6 indicated a difference of approximately one net charge between human and porcine C3a, with the human anaphylatoxin exhibiting the more basic behavior. Although the amino acid compositions are similar, significant differences exist. The most marked difference was the total absence of threonine residues in porcine C3a. The NH2-terminal sequences of 20 amino acid residues were examined; homology existed for 16 of the 20 positions. Although partial analysis of the primary structure of human and porcine C3a indicates approximately 80% homology, no immunological cross-reactivity between the anaphylatoxins could be detected with antisera produced to either human or porcine C3a. In spite of the structural differences, the biological activities of porcine and human C3a were essentially identical. Smooth muscle contraction, increase in vascular permeability, and release of histamine from mast cells were similarly induced by equal amounts of anaphylatoxin from either human or porcine origin. Porcine C3a, like human C3a, was shown to contain a COOH-terminal arginyl residue essential for smooth muscle contraction and for induction of histamine release from mast cells. The sequence adjacent to the COOH-terminal arginine was Leu-Ala-Arg-COOH for both humans and porcine C3a. Current evidence suggests common mechanisms exist for the generation of C3a in various animal species and that the two known C3 activating enzymes in serum exhibit trypsin-like specificity.

Amino Acid Sequence↗

Effect of low-dose citrate anticoagulation on the clinical safety and efficacy of direct adsorption of lipoproteins (DALI apheresis) in hypercholesterolemic patients: a prospective controlled clinical trial.

Direct adsorption of lipoproteins (DALI) is the first lipid apheresis system compatible with whole blood with the advantage of a very simple procedure. A mixture of heparin plus citrate (ACD-A) is used for the anticoagulation regimen (AR). A clinical, prospective, controlled crossover study was performed to test the safety and efficacy of low-dose citrate (LDC) anticoagulation in DALI. Five chronic DALI patients suffering from coronary heart disease and hypercholesterolemia underwent 3 DALI sessions each using the LDC anticoagulation regimen (60 IU heparin/kg body weight as initial bolus; 1:40 ACD-A: blood as perfusion). This was compared to 3 sessions per patient with the standard AR (bolus of 20 IU heparin/kg, 1:20 ACD-A as perfusion). Patient blood volumes (1.6; average of 7,040 ml) were treated with 750 ml adsorber gel per session at a blood flow rate of 60 ml/min. Mean LDL and Lp(a) reductions exceeded 60% with both AR. No clinical side effects were observed. Both AR controlled the coagulation well as evidenced by a sufficient prolongation of the partial prothrombin time (PTT) and activated clotting time as well as low thrombin-antithrombin (TAT) formation. Biocompatibility parameters exhibited favorable results (low activation of complement and cells, and only slight formation of C3a, C5a, beta-thromboglobulin, elastase, and TNF-alpha). The asymptomatic bradykinin generation was comparable in both study arms. LDC optimized the ionized calcium levels and pH in the efferent blood postadsorber. LDC anticoagulation was safe and effective, and may further improve the tolerance of DALI apheresis in hypercholesterolemic patients.

Adsorption↗

Pharmacokinetics, toxicity, and efficacy of ends-modified raf antisense oligodeoxyribonucleotide encapsulated in a novel cationic liposome.

Raf-1 protein serine threonine kinase plays an important role in cell survival and proliferation. Antisense inhibition of Raf-1 expression has been shown to enhance the cytotoxic effects of radiation and anticancer drugs. Here we have evaluated the toxicity, pharmacokinetics, and antitumor efficacy of a novel formulation of liposome-entrapped raf antisense oligodeoxyribonucleotide (LErafAON). The LErafAON preparation showed high liposome entrapment efficiency of rafAON (>85%) and stability at room temperature. In CD2F1 mice, administration of LErafAON produced no morbidity/mortality (5-35 mg/kg/dose, i.v., x12). Dose-related elevations in liver enzymes (alanine aminotransferase and aspartate aminotransferase) and histopathological changes in liver were noted in LErafAON and blank liposome groups. No morbidity/mortality and changes in clinical chemistry or histopathology were observed in New Zealand white rabbits (3.75 mg/kg/dose, i.v., x8; 6.5 mg/kg/dose, i.v., x6) or in cynomolgous monkeys (3.75 or 6.25 mg/kg/dose, i.v., x9). Transient decrease in total hemolytic complement activity (approximately 62-74%) and increases in C3a (approximately 3-fold) and Bb levels (approximately 5-12-fold) were observed in LErafAON and blank liposome groups of monkeys. A 30 mg/kg i.v. dose of LErafAON in human prostate tumor (PC-3)-bearing BALB/c athymic mice gave a terminal plasma half-life of 27 h, and intact rafAON could be detected in plasma and in normal and tumor tissues for up to at least 48 h. In monkeys, the terminal plasma half-life of 30.36 +/- 23.87 h was observed at an i.v. dose of 6.25 mg/kg. LErafAON (25 mg/kg/dose, i.v., x10) or ionizing radiation (3.8 Gy/day, x5) treatment of PC-3 tumor-bearing athymic mice led to tumor growth arrest, whereas a combination of LErafAON and ionizing radiation treatments resulted in tumor regression. LErafAON treatment caused inhibition of Raf-1 protein expression in normal and tumor tissues in these mice (>50%, versus controls). These data have formed a basis of the clinical Phase I studies of LErafAON for cancer treatment.

Animals↗

Anatomic, physiologic, bacteriologic and immunologic aspects of peritonitis.

The anatomic aspect of peritonitis describes the division of the abdominal cavity into the supracolic, infracolic and paracolic spaces, moreover the lesser sac and the cul-de-sac of the pelvis. Physiologically the peritoneum plays an important role in the passive exchange of fluid and absorption of particles. Endotoxin, which is elaborated by bacteria activates the classical as well as the alternative complement pathway. It activates also the arachidonic acid metabolism, leading to the release of prostaglandins (PG) and leukotriens (LTC). The local host defense against a bacterial invasion includes the activation of cellular and humeral immunologic defense mechanism, in which the final product of the complement pathway (C5b-9), as well as chemoattractants C3a, C5a and C567 play a key role.

Abdomen↗

Complement activation products and factors influencing phagocyte migration in synovial fluids from children with chronic arthritis.

Synovial fluids from children with chronic arthritis were examined simultaneously for the presence of complement activation products and factors affecting phagocyte migration. The concentrations of C3a and C5a, but not C4a, were found to be elevated relative to normal plasma. However, the C3a and C5a concentrations in synovial fluid did not correlate with C1q binding values or with degree of migration inhibition or chemoattraction caused by that fluid. Although this data implies complement activation occurs in inflamed joints in juvenile arthritis, the specific role of immune complexes remains unproven.

Arthritis, Juvenile↗

Evaluation of leukocyte adhesion on polyurethanes: the effects of shear stress and blood proteins.

Leukocytes are a central cell type in directing host inflammatory and immune processes; thus, its response to biomaterials is extremely important in understanding material-host interaction. Blood contacting biomaterials may activate the complement cascade, thus promote leukocyte adhesion and activation to the biomaterial surface. We hypothesize that the extent of complement-mediated leukocyte activation is modulated by the material chemical formulation and the presence of fluid shear stress. Medical-grade polyurethanes with or without 4,4'-butyldiene bis(6-tert-butyl-m-cresol) antioxidant additives and a rotating disk system were utilized to study cell adhesion under a well-characterized shear stress field. Radioimmunoassay and ELISA were employed to assess the extent of complement activity. The results showed that adherent leukocyte densities decreased with increasing shear stress and that leukocyte adhesion was decreased significantly further by the presence of the antioxidant in the polyurethanes. Cell adhesion under flow conditions was abolished when complement C3 protein was depleted from the test medium. An increase in complement Factor H adsorption was observed at high shear region; however, no change in the complete complement activation was observed in the presence of shear stress as indicated by the protein S-terminal complement complex level. Based on these results, oligopeptides designed from C3a, C5a, and fibronectin were grafted onto a cell-nonadhesive polymer surface to probe the molecular mechanisms of leukocyte adhesion as mediated by protein-receptor complexation. The results showed that C3a-derived peptides mediated higher adherent macrophage density when compared to that mediated by C5a- and fibronectin-derived peptides.

Biocompatible Materials↗