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PubMed1990

Isolation and characterization of a complement-activating lipid extracted from human atherosclerotic lesions.

The major characteristics of human atherosclerotic lesions are similar to those of a chronic inflammatory reaction, namely fibrosis, mesenchymal cell proliferation, the presence of resident macrophages, and cell necrosis. Atherosclerosis exhibits in addition the feature of lipid (mainly cholesterol) accumulation. The results of the present report demonstrate that a specific cholesterol-containing lipid particle present in human atherosclerotic lesions activates the complement system to completion. Thus, lipid could represent a stimulatory factor for the inflammatory reaction, whose underlying mechanistic basis may be, at least in part, complement activation. The complement-activating lipid was purified from saline extracts of aortic atherosclerotic lesions by sucrose density gradient centrifugation followed by molecular sieve chromatography on Sepharose 2B. It contained little protein other than albumin, was 100-500 nm in size, exhibited an unesterified to total cholesterol ratio of 0.58 and an unesterified cholesterol to phospholipid ratio of 1.2. The lipid, termed lesion lipid complement (LCA), activated the alternative pathway of complement in a dose-dependent manner. Lesion-extracted low density lipoprotein (LDL) obtained during the purification procedure failed to activate complement. Specific generation of C3a desArg and C5b-9 by LCA indicated C3/C5 convertase formation with activation proceeding to completion. Biochemical and electron microscopic evaluations revealed that much of the C5b-9 present in atherosclerotic lesions is membraneous, rather than fluid phase SC5b-9. The observations reported herein establish a link between lipid insudation and inflammation in atherosclerotic lesions via the mechanism of complement activation.

Aorta↗

PubMed2004

Assessment of complement activation during membrane-based plasmapheresis procedures.

Previous studies have suggested that plasmapheresis procedures using a separation membrane may activate the complement system and release anaphylatoxins. This study determines the content in C3a/C3a(des Arg) and C5a/C5a(des Arg) in plasma donations obtained by the new Haemonetics Filter Core (FC) procedure and compares it to Baxter Autopheresis C (Auto-C). FC performs sequential blood centrifugation and plasma filtration on a microporous polyethersulfone membrane, while Auto-C removes blood cells by simultaneous gravitation and filtration on a rotating nylon membrane. One group of 34 donors donated on FC and two groups of 30 and 10 donors on Auto-C. Plasma aliquots were taken from the plasma units within 30 min of the end of the collection procedures, frozen at < -30 degrees C and assessed for C3a and C5a at various time points of storage. Mean C3a/C3a(des Arg) in FC plasma (N = 34) was 1,151 (range: 526-2,991), 1,092 (range: 349-3498), and 507 (range: 307-815) ng/ml at time of collection and after 6 and 12 months of storage, respectively. Respective C5a/C5a(des Arg) was 26.6 (range 4.9-74), 18.9 (9.5-42.6), and 30.9 (range: 10.7-62.3) ng/ml. Mean C3a/C3a(des Arg) was higher in Auto-C (P < 0.001): 4,724 ng/ml (N = 10; range: 2,400-7 ,360) and > 4,149 ng/ml (N = 30; 2,408- > 6,430) after 3 and 18 months storage, respectively. Mean C5a/C5a(des Arg) was 32.1 ng/ml (N = 30; range: 10.6-57.2) after 18 months of storage. Complement activation in FC plasmas appears limited compared to Auto-C, suggesting better biocompatibility of this collection device and/or a favourable impact of the sequential cell centrifugation/filtration technology used. Further studies are needed to explain differences in complement activation between apheresis procedures and to assess clinical impacts, if any.

Complement Activation↗

PubMed1992

C3a receptor on dibutyryl-cAMP-differentiated U937 cells and human neutrophils: the human C3a receptor characterized by functional responses and 125I-C3a binding.

The anaphylatoxic peptide C3a is part of a basic immunological defense mechanism, the complement system. Research on the human C3a receptor and signal transduction is hampered by the lack of a suitable human cell or cell line. We screened tumor cell lines and human blood cells for a C3a-dependent increase in cytosolic Ca2+ ([Ca2+]i) and analyzed this reaction in a fura-2/AM fluorescence assay for cells in suspension. U937 cells, when differentiated with dibutyryl-cAMP (Bt2cAMP), and purified human neutrophils reacted in a dose-dependent fashion to C3a and a C3a analogue synthetic peptide. We found complete homologous desensitization of this response and no heterologous desensitization to human C5a. Pertussis toxin totally blocked the increase in [Ca2+]i, indicating the possible involvement of a G-protein. Single-cell analysis by digital imaging fluorescence microscopy indicated that neutrophilic granulocytes responded to C3a. In binding studies with Bt2cAMP-differentiated U937 cells and human granulocytes, the 125I-C3a binding was displaced by C3a, yielding one class of C3a binding sites with dissociation constants (Kd) in the low nanomolar range. We identified myo-inositol 1,4,5-trisphosphate (IP3) as the second messenger possibly causing the [Ca2+]i increase and the release of N-acetyl-beta-D-glucosaminidase as one secretory cell response. By functional and binding studies we demonstrated the expression of the C3a receptor on Bt2-cAMP-differentiated U937 cells and human neutrophils and characterized parts of the C3a signal pathway. Our data support a physiological concept in which C3a might be more important than presently thought.

Acetylglucosaminidase↗

PubMed2002

Inflammatory mediator removal by zero-balance ultrafiltration during cardiopulmonary bypass.

The abnormal conditions to which blood is subjected during cardiopulmonary bypass (CPB) trigger an activation of the inflammatory response in all patients to varying degrees. Both complement activation and the release of cytokines characterize this response. Most inflammatory mediators have a molecular weight that is below the membrane pore size of commonly used ultrafilters, which should allow them to be freely filtered. However, some mediators have been shown to fail to cross through the membrane even though they are small enough to cross. The purpose of the present study was to determine whether certain inflammatory mediators could be removed by ultrafiltration when performed during the rewarming phase of CPB. Thirty adult patients undergoing a single, open-heart procedure were randomized to either control (no ultrafiltration) or to the zero-balance ultrafiltration (ZBUF) group. ZBUF was performed by removing 3 l/m2 blood using a 65-kDa ultrafilter with 1.3-m2 surface area. A volume of a balanced salt crystalloid solution (Plasmalyte) equal to the filtered blood volume was given to replace the fluid removed. Patient data was taken before CPB (T1), immediately following CPB (T2), and 12 h following the procedure (T3). The average volume of filtrate removed during ZBUF was 6405 ml, which was analyzed for the presence of interleukin (IL)-1, IL-6, tumor necrosis factor-alpha (TNF-alpha), C3a, and C5a. The average concentrations of the mediators measured in the effluent were: IL-1, 0.17 pg/ml; IL-6, 0.64 pg/ml; TNF-alpha, 1.25 ng/ml; C3a, 782.6 ng/ml; C5a, 25.6 ng/ml. In every case except for IL-1, the amounts of mediators removed were significantly greater than zero. This study demonstrates that ultrafiltration is a strategy that can be used during CPB in the adult to remove significant amounts of inflammatory mediators.

Adult↗

PubMed2001

Biocompatibility of hemodialysis membranes: interrelations between plasma complement and cytokine levels.

Hemodialysis (HD) membrane biocompatibility is defined as absence of complement activation. We have recently shown that circulating levels of interleukin (IL) 1 and IL-2 predict death and survival, respectively, of HD patients. Studies have assessed IL-1 in treatments with biocompatible and less biocompatible dialysis membranes, but no study has correlated circulating levels of all these immunoreactants. We assessed these immunoreactants, and temperature as an outcome, during HD in patients treated with different membranes. Twelve stable patients, receiving thrice-weekly chronic bicarbonate HD, were randomly dialyzed with three different types of membranes, composed of: Cuprophan, cuprammonium rayon modified cellulose, and Hemophan. Blood was drawn from the arterial line port before (Pre) and 15, 30, and 60 min during and after (Post) HD. Patients' temperatures were measured before and after each treatment. The plasma concentrations of IL-1 and IL-2 and factors C3a and C5a were assessed by ELISA. There were no differences between baseline levels of any of the immunoreactants in patients treated with different dialyzers. C3a, C5a, and IL-1 levels increased significantly during HD treatments with all three different membranes. C3a, C5a, and IL-1 levels during Cuprophan and Hemophan treatments were significantly higher than the levels during modified cellulose treatment at 30 and 60 min and Post (p < 0.01). For all the immunoreactants, however, the Post levels were higher than the Pre levels. In contrast to IL-1, there were no differences in mean IL-2 levels during treatments when different membranes were compared. There were few correlations of plasma C3a and C5a levels with plasma IL-1 levels, but there was only one treatment time in one dialyzer group during which IL-2 and any of the other factors were correlated. Pre and Post temperature values and percent change in temperature were not correlated with any of the immunoreactants measured. These data show that C3a, C5a, and IL-1 responses are similar, but not identical, during treatments with different membranes. The response of circulating IL-2 levels to treatments is quite different from that of plasma C3a, C5a and IL-1 levels and suggests that these changes are not solely due to treatment factors. Treatment with modified cellulose membranes is associated with a different immunoreactive profile as compared with patients dialyzed using other cellulose membranes. We suggest that circulating IL-1 levels are good biocompatibility markers.

Adult↗

PubMed1984

Complement activation during hemodialysis: clinical observations, proposed mechanisms, and theoretical implications.

Human C3a radioimmunoassay techniques were employed to define both the temporal profile and the amount of complement activation taking place in the extracorporeal circuit during maintenance hemodialysis. Prospective studies demonstrated that C3a formation, like hemodialysis-associated leukopenia, was a transient phenomenon that occurred predominantly during the first 30 min of dialysis. Quantitative comparisons revealed that new Cuprophan hemodialyzers displayed somewhat greater complement-activating potential than cellulose acetate dialyzers. By contrast to new Cuprophan membranes, both reused Cuprophan and polyacrylonitrile dialyzers exhibited only a modest ability to activate human complement. These findings are compatible with the known mechanisms of complement activation and suggest that certain chemical and biochemical methods might be exploited to enhance the biocompatibility of cellulose dialysis membranes.

Acrylic Resins↗

PubMed1988

Complement C3 and C5 degradation products during hemodialysis treatment: study of an index of membrane bioincompatibility.

In 10 hemodialyses (HD) with cuprophan (CU) and 10 with polyacrylonitrile (PAN), signs of complement activation were investigated by following arterial and venous levels of C3a, C3d and C5a, in order to propose a marker of bioincompatibility. Despite large individual variabilities, significant increases of these molecules were detected at t 20 min, particularly with CU device in the artery and more marked in the vein except for C3d with PAN. During the later stage of HD, while C3a and C5a levels gradually declined, but remained significantly higher than t 0 in all the patients treated with CU, the C3d concentration reached a plateau suggesting a continuous complement activation throughout HD. HD using PAN membranes were associated with a lower C3a, C3d and C5a generation and fewer dialyses generating these products. In some dialyses the higher arterial level of these molecules suggests an extra-dialyzer complement activation especially with PAN membrane. Although C5a venous levels appeared to be the more significant index of complement activation, for clinical purposes we propose the C3d arterial measurement as a reliable, non-expensive and technically simple indicator of membrane intolerance.

Acrylic Resins↗

PubMed1992

Effects of extraerythrocytic hemoglobin and its components on mononuclear cell procoagulant activity.

Earlier studies performed in rabbits in this laboratory showed that human hemoglobin causes leukocyte infiltration into heart and lung tissues and coagulation abnormalities including thrombosis. Since stimulation of peripheral blood mononuclear cells induces procoagulant activity, we investigated the possibility that isolated peripheral blood mononuclear cells from humans and rabbits were stimulated by hemoglobin to produce a procoagulant activity response. Stroma-free hemoglobin and its purified components were assayed for their stimulatory effect on peripheral blood mononuclear cells. The added effect of endotoxin contamination was also explored. A significant dose-dependent effect of stroma-free hemoglobin on procoagulant activity was found with both human and rabbit peripheral blood mononuclear cells, but rabbit cells were found to be 50-fold more sensitive than human cells. Hematin, methemoglobin, and purified hemoglobin Ao elicited procoagulant activity effects with human peripheral blood mononuclear cells, but isolated globin did not. We also studied the effects of these compounds on activation of complement, a known mediator of the procoagulant activity response. Stroma-free hemoglobin, hematin, purified hemoglobin Ao, and methemoglobin were all found to cleave complement fraction C3 to C3a but at concentrations much higher than those required for procoagulant activity. The data suggest that heme itself may be responsible for the procoagulant effect of stroma-free hemoglobin solutions.

Animals↗

PubMed1999

[Effect of complement on the production of tumor necrosis factor alpha by human leukocytes with culture supernatants of clinical isolates of Staphylococcus aureus].

Induction of tumor necrosis factor alpha (TNF-alpha) of human leukocytes by overnight culture supernatants of Staphylococcus aureus (S. aureus) (CS) (4 strains) and then the effect of the complement on production of TNF alpha by the treated cells were examined. One-tenth diluted solution of CS was added to Heparinized blood and was incubated for 6 hrs at 37 C in a 5% CO-air humidified incubator. TNF alpha level in the plasma was measured by ELISA. The level in the plasma was different in different CS. The induction of TNF alpha was not found in EDTA-added blood but was found in the EGTA-added them treated with CS, though different levels were showed. Western blotting assay of these plasma samples without EDTA-added blood found the presence of both C5a and C3a. Neither C5a and C3a was found in Heparinized blood treated with a relative concentration to TSST-1, enterotoxin C and alpha (alpha) homolysin contained in CS. Mixture of these toxins induced only 1/6.5 of the TNF alpha amount obtained with the CS. Human leukocytes isolated by Mono.-Poly. resolving solution were cultured with CS in RPMI 1640 medium with or without 10% fresh or heated serum. Production of TNF alpha by the isolated leukocytes was not found under the condition of serum free. But it was found in the presence of fresh serum and also in the presence of heated serum. The addition of CS to RPMI 1640 containing heated serum did not occur naturally in the production of C5a. These results suggest that there is a difference in TNF alpha inductivility to human leukocytes in each strain and that other bacterial components without TSST-1, SEC and alpha-hemolysin are more important to induce TNF alpha. Serum may be necessary to produce TNF alpha by CS-treated cells as a source of factor(s) to interact with bacterial components rather than a source of complement.

Cells, Cultured↗

PubMed1987

[Complement activation following head and brain trauma].

The prognosis for a patient with a severe head injury is dependent not only upon the location and the degree of this trauma, but also upon additional complications. For example, disseminated intravascular coagulation (DIC) can occur because of the thromboplastic activity of the damaged brain tissue that enters the circulation. The complement (C) system is activated by certain enzymes that cleave the clotting factors. Therefore, after head injuries we searched for C activation because it could result in the adult respiratory distress syndrome (ARDS). Patients and methods. We had two groups of patients: (1) 23 with large destruction and (2) 13 with little destruction of the brain tissue. Eighteen patients in group 1 and 8 in group 2 had isolated brain trauma. Blood samples were taken--upon arrival at the hospital and then 1, 3, 7, 12, 24, and 48 h later; after that we took weekly blood samples up to the completion of their treatment in the intensive care unit. We measured the total hemolytic serum C activity (CH50), activation of alternative pathway hemolysis (APH50), cleavage products C3a and C3d, and total protein. Furthermore, we studied the coagulation parameters of the extrinsic (prothrombin time) and intrinsic (partial thromboplastin time) pathways and fibrinogen content. From the patients records we extracted clinical parameters such as neurological status, intracranial pressure, pathological details on computer tomography hemoglobin and arterial-alveolar oxygen difference. Results. Figure 1 shows the different reactions of the C system in both groups: while patients of group 1 suffered from a decrease in total and alternative hemolytic activity, the other group increases in both parameters.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1985

Increased anaphylatoxins (C3a and C4a) in psoriatic sera.

We measured C3a and C4a anaphylatoxins in the serum of 56 psoriatic patients and 36 healthy control subjects by radioimmunoassay in order to clarify the mechanism of complement activation occurring in psoriatic lesions. Whereas a small amount of anaphylatoxins were demonstrable even in the sera of healthy adults, the serum concentrations of C3a and C4a anaphylatoxins were significantly higher in psoriatic patients than those in non-psoriatic controls. The increased serum anaphylatoxin levels did not correlate well with either the extent or the activity of the skin lesions, but a comparison of anaphylatoxin levels in 10 patients before and after successful treatment of skin lesions showed that the serum anaphylatoxin levels decreased with improvement of the skin lesions. Our results suggest that complement activation takes place in psoriatic patients chiefly via the classical pathway.

Adolescent↗

PubMed2006

Antifungal activity of C3a and C3a-derived peptides against Candida.

Antimicrobial peptides are generated during activation of the complement system [Nordahl et al. Proc. Natl. Acad. Sci. U. S. A. 2004, 101:16879-16884]. Here we show that the anaphylatoxin C3a exerts antimicrobial effects against the yeast Candida. Fluorescence microscopy and electron microscopy analysis demonstrated that C3a-derived peptides bound to the cell surface of Candida, and induced membrane perturbations and release of extracellular material. Various Candida isolates were found to induce complement degradation, leading to generation of C3a. Arginine residues were found to be critical for the antifungal and membrane breaking activity of a C3a-derived antimicrobial peptide, CNY21 (C3a; Cys57-Arg77). A CNY21 variant with increased positive net charge displayed enhanced antifungal activity. Thus, C3a-derived peptides can be utilized as templates in the development of peptide-based antifungal therapies.

Amino Acid Sequence↗

PubMed1992

Complement activation and polymorphonuclear neutrophil leukocyte elastase in sepsis. Correlation with severity of disease.

Complement activation is necessary for an adequate immune and inflammatory response to infections. Activation releases anaphylatoxins that cause vasodilation, increase vascular permeability, and trigger release of polymorphonuclear neutrophil leukocyte (PMN) lysosomal enzyme and oxygen radicals. Under normal circumstances, an orderly progression of such events has a beneficial antimicrobial effect. The same mechanism, however, when uncontrolled, may damage host tissues. To provide information about the clinical importance of such events in sepsis, different complement parameters (C3, C4, and the desarginated forms of C3a [C3a(des)-Arg] and C5a [C5a(des)-Arg]), PMN elastase, and malondialdehyde (a by-product of membrane peroxidation by oxygen radicals) were measured daily in 26 septic patients and correlated with two objectively assessed and previously validated severity scores (acute physiology and chronic health evaluation [APACHE II] and Sepsis Severity Score [SSS]). Nonsurvivors (n = 12) had significantly greater and longer lasting complement activation than that in survivors, as reflected by higher levels of catabolic peptides (C3a(des)-Arg) and lower levels of native proteins (C3 and C4). C3a(des)-Arg, C3, C4, and the C3a(des)-Arg-C3 ratio were correlated with Sepsis Severity Scores. Polymorphonuclear neutrophil leukocyte elastase levels were higher in nonsurvivors and were correlated with C3a(des)-Arg and the C3a(des)-Arg-C3 ratio. Malondialdehyde levels were significantly higher in all patients than in controls, without, however, any relationship to severity of disease or clinical outcome. Since the higher and more persistent the complement activation and polymorphonuclear neutrophil leukocyte stimulation, the worse the patient's prognosis, we conclude that these mechanisms may be important in the clinical development of sepsis.

Adult↗

PubMed2006

Complement and demyelinating disease: no MAC needed?

It has long been accepted that the complement system participates in the onset, evolution, and exacerbation of demyelinating disease, and it is widely suspected that this is accomplished mainly via destruction of nervous tissue by membrane attack complex (MAC)-mediated lysis of oligodendrocytes and neurons. However, recent studies using mutant mice indicate the MAC may not be so important. For example, mice lacking C5 and mice lacking the C5a receptor both develop experimental autoimmune encephalomyelitis (EAE) with the same frequency and intensity as their wild type counterparts. Also, transgenic mice that express C5a exclusively in the central nervous system (CNS) develop EAE that is not remarkably different from that in non-transgenic littermates. Since C5 is required for formation of the MAC, development of fulminant EAE in the absence of this complement protein demonstrates that non-complement-mediated mechanisms of CNS damage are operating. Paradoxically, mice lacking C3, mice lacking the C3a receptor, and mice lacking the complement receptor type 3 develop attenuated EAE, while mice that express C3a exclusively in the CNS develop severe and often fulminant EAE. Based on these newer data, we posit that C3-derived biologically active fragments, rather than C5 and the MAC, are central players in the pathophysiology of complement in EAE.

Animals↗

PubMed1998

Both C3a and C3a(desArg) regulate interleukin-6 synthesis in human peripheral blood mononuclear cells.

Synthesis of complement components is part of the acute-phase response. Interleukin-6 (IL-6) is a critical mediator of the acute-phase response during infections and injuries. Plasma levels of C3a and IL-6 have been proposed as prognostic indicators in sepsis and trauma. The effects of C3a and C3a(des)Arg on IL-6 gene expression and protein production in human peripheral blood mononuclear cells (PBMC) were investigated. Neither C3a nor C3a(des)Arg alone induced detectable IL-6 protein or mRNA levels. However, C3a and C3a(des)Arg affected endotoxin-induced IL-6 synthesis in a dose-dependent manner. In nonadherent PBMC, C3a or C3a(des)Arg suppressed, while in adherent PBMC, C3a or C3a(des)Arg enhanced IL-6 protein and mRNA levels. These results suggest that C3a and C3a(des)Arg may provide a control mechanism of acute-phase responses by enhancing IL-6 synthesis in adherent monocytes at local inflammatory sites and by inhibiting IL-6 synthesis in circulating monocytes.

Cell Adhesion↗

PubMed1989

C3a-induced contraction of guinea pig ileum consists of two components: fast histamine-mediated and slow prostanoid-mediated.

Guinea pig ileum is the classical experimental model for assessing the biological activity of complement-derived anaphylatoxins. Nevertheless, it is still at issue whether C3a-induced ileal contraction is entirely dependent on histamine release. We report that the contraction of the intestinal smooth muscle in response to C3a is characterized by two components, fast and slow, whose incidence and amplitude is strictly dependent on C3a concentration; the larger the concentration of C3a, the greater the incidence and magnitude of the fast component and the less frequent the slow component. The fast and slow components were characterized by a sigmoid and bell-shaped concentration-response curve, respectively. The fast component was associated with the release of endogenous histamine, increased in magnitude with the quantity of histamine released and was prevented by the histamine H1 receptor antagonist pyrilamine. On the contrary, there was no correlation between the quantity of histamine released by C3a and the magnitude of the slow component. Instead, the slow component was associated with the release of PGE2 and was prevented by the cyclooxygenase inhibitor indomethacin. Neither component was affected by the leukotriene receptor antagonist FPL 55712. Our data indicate that C3a-induced ileal contraction is partially histamine dependent in that histamine mediates only the fast component, whereas cyclooxygenase metabolites are responsible for the slow component.

Animals↗

PubMed1983

Symptoms and activation of granulocytes and complement with two dialysis membranes.

Complement (C) activation, neutropenia, and mild pulmonary dysfunction attend hemodialysis (HD) with cellophane [for example, cuprophan (Cu)] membranes. While usually asymptomatic, these phenomena may cause distress in patients with cardiopulmonary disease, and "start-up" symptoms of HD might be mediated by C-stimulated granulocytes (PMNs). Cellulose acetate (CA) hemodialysis membranes have been devised and claimed more blood compatible than Cu. In a blinded series of HD patients, pruritus, fatigue, and sense of well-being were each scored statistically more favorably by the patients during HD with CA than during HD with Cu (P less than 0.05). Postulating that less C activation might underlie the benefit, we showed that neutropenia was less severe with CA (nadir 77.6% of initial count, +/- 4 SEM) than with Cu (38.3% +/- 2.9; P less than 0.01). In vitro, incubation of CA membranes with plasma led to less C3 conversion (20% vs. 40%), less PMN aggregating activity (5.9 ZAP units vs. 36.3) and less decrement in CH50 (6.5% vs. 22%) than like incubations of Cu. C activation was also less potent in vivo: During HD plasma C3a rose from a mean 401 ng/ml to a peak 6,325 in patients on Cu dialyzers, but from 426 to only 3,637 in patients on CA devices (P less than 0.05). Time-course studies suggested CA was initially as potent an activator as Cu but rapidly lost ability to activate C, possibly because of saturation of C3b binding sites. As an index of PMN activation, we also assayed plasma lactoferrin and found levels significantly higher during Cu than CA dialysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Anaphylatoxins↗

PubMed1985

Activation of the alternative complement pathway by intraocular lenses.

To determine if posterior chamber polymethylmethacrylate lenses with polypropylene loops activate complement, the authors measured levels of C3a, C4a and C5a by radioimmunoassay in human sera incubated with and without these lenses. Human sera incubated with intraocular lenses showed elevated levels of C3a and C5a but no change in C4a. There were no statistically significant differences in the generation of activated complement by polypropylene loops vs polymethylmethacrylate optics. The authors also compared the ability of intraocular lenses to activate complement with that of zymosan and endotoxin, known activators of the alternative pathway. Our results suggest that polymethylmethacrylate lenses with polypropylene loops generate C3a and C5a by activation of the alternative complement pathway.

Adult↗