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PubMed1990

Association of a 38 kDa bovine serum protein with the outer membrane of Bordetella pertussis.

Upon cultivation of Bordetella pertussis in bovine serum, a 38 kDa protein was found to be tightly associated with the outer membrane. The intensity of the 40 kDa porin was reduced under these growth conditions. Exposure of Bordetella pertussis, grown in Stainer and Scholte medium, to bovine serum for 1 h did not result in the appearance of the 38 kDa protein. Unlike the 40 kDa porin however, the electrophoretic mobility of this protein was affected neither by temperature of denaturation nor by the presence of 2-mercaptoethanol. Amino acid sequence analysis of the N-terminal of the 38 kDa protein revealed that his protein had 87% homology to both the mouse and human complement C3 precursors.

Amino Acid Sequence↗
PubMed1993

Progesterone and dexamethasone inhibition of estrogen-induced synthesis of DNA and complement in rat uterine epithelium: effects of antiprogesterone compounds.

Progesterone (P) blocks estrogen induction of cell proliferation and synthesis of complement C3 in the epithelium of the immature rat uterus. Here it is shown that dexamethasone (Dex) exerts a similar inhibitory effect on these two parameters. Furthermore, analysis of the newly synthesized, secreted proteins produced during a 20 h explant culture period showed that not only does the uterus synthesize complement C3 but it is capable of proteolytically cleaving complement into its biologically active peptides. Since large doses of P are required for its inhibitory effects and since P can interact with the glucocorticoid receptor (GR), the role of the GR in mediating the P effect was questioned. Two antiprogesterone compounds with reportedly differing antiglucocorticoid activity, ZK98.734 and RU486, were tested for their ability to antagonize the inhibitory actions of P and Dex. Attenuation of estrogen-induced epithelial DNA synthesis by either P or Dex was fully overcome by concurrent administration of either ZK98.734 or RU486. On the other hand, while either antagonist was effective against the inhibitory action of P on estrogen-induced complement C3 synthesis, only ZK98.734 was fully effective in blocking inhibition by Dex. Thus, unlike its activity in rat hepatic cells, ZK98.734 is a potent antiglucocorticoid in the immature rat uterus. Because of this antiglucocorticoid activity, differential antagonism of the P response was not possible using these two steroid analogs. Although these observations support the notion of GR mediated inhibition of estrogen action in the uterus, they do not answer the question of whether P might act through a GR mediated pathway.

Animals↗
PubMed1993

Antiandrogenic property of RU 486: enhancement of estrogen-induced uterine peroxidase activity in the rat.

The contragestational steroid RU 486 enhanced the increase in peroxidase activity produced by estradiol in estrogen-primed immature rat uteri and, like the antiandrogen flutamide, RU 486 reversed the inhibitory effect of testosterone on this estrogen-induced response. It antagonized the inhibition produced by progesterone but had no effect on peroxidase induction by itself or in unprimed immature animals. RU 486 also enhanced the effect of estradiol on the synthesis of complement component C3 in the rat uterus. The results confirm that RU 486 possesses antiandrogenic as well as antiprogestational properties. They also suggest that, in normal adult animals, the increase in peroxidase activity in the uterus in response to estrogen is not expressed fully but held in check by other endogenous steroids acting through their individual receptors.

Animals↗
PubMed1994

Complement C3, eosinophil cationic protein and symptom evaluation in interstitial cystitis.

Interstitial cystitis is a painful, irritative voiding dysfunction of unknown etiology. In this study 19 women undergoing treatment for interstitial cystitis and 6 healthy women of similar age provided 2 urine and serum specimens with at least a 3-month interval between collections. Complement C3 and eosinophil cationic protein were determined by immunoassay methods, and symptom severity was quantitated with a visual analog scale questionnaire. Concentrations of complement C3 and eosinophil cationic protein from either serum or urine were not significantly different between interstitial cystitis patients and controls at either determination, although substantial differences were noted even between individual initial and followup determinations. Normalization of urine osmolality did not alter these results. Symptom severity scores were significantly greater in interstitial cystitis patients compared to controls but failed to correlate with the concentrations of complement C3 or eosinophil cationic protein. Therefore, the hypothesis that complement C3 and eosinophil cationic protein may be etiological factors of interstitial cystitis is not supported.

Adult↗
PubMed2002

Structural features of immunologically active polysaccharides from Ganoderma lucidum.

Three polysaccharides, two heteroglycans (PL-1 and PL-4) and one glucan (PL-3), were solubilized from the fruit bodies of Ganoderma lucidum and isolated by anion-exchange and gel-filtration chromatography. Their structural features were elucidated by glycosyl residue and glycosyl linkage composition analyses, partial acid hydrolysis, acetolysis, periodate oxidation, 1D and 2D NMR spectroscopy, and ESI-MS experiments. The data obtained indicated that PL-1 had a backbone consisting of 1,4-linked alpha-D-glucopyranosyl residues and 1,6-linked beta-D-galactopyranosyl residues with branches at O-6 of glucose residues and O-2 of galactose residues, composed of terminal glucose, 1,6-linked glucosyl residues and terminal rhamnose. PL-3 was a highly branched glucan composed of 1,3-linked beta-D-glucopyranosyl residues substituted at O-6 with 1,6-linked glucosyl residues. PL-4 was comprised of 1,3-, 1,4-, 1,6-linked beta-D-glucopyranosyl residues and 1,6-linked beta-D-mannopyranosyl residues. These polysaccharides enhanced the proliferation of T- and B-lymphocytes in vitro to varying contents and PL-1 exhibited an immune-stimulating activity in mice.

Adjuvants, Immunologic↗
PubMed1984

Basic proteins bind immunoglobulin G: a mechanism for demyelinating disease?

Heat-aggregated immunoglobulin G ( HAGG ) bound avidly to solid-phase basic proteins, including myelin basic protein. In contrast, monomeric immunoglobulin bound weakly. Bound HAGG could activate complement. Normal human serum strongly inhibited the binding of HAGG , even when decomplemented or greatly diluted. Cerebrospinal fluid was also inhibitory, but the effect was weaker. Apart from inhibition by decomplemented serum, the biochemical characteristics of the interaction were similar to those of other Fc ligands with IgG, particularly C1q. In multiple sclerosis this interaction could occur between IgG and central-nervous-system myelin basic protein, leading to demyelination by activation of immune mechanisms of tissue damage. Bound IgG is present in multiple sclerosis plaques and IgG from multiple sclerosis patients can produce demyelination in experimental models. However, there is little evidence of any specific immunity to central-nervous-system antigens in multiple sclerosis, and this non-specific interaction might be an important link in the pathogenesis of the disorder.

Blood↗
PubMedDate not supplied

Stagnant versus dynamic conditions: a comparative adsorption study of blood proteins.

Haemodynamic parameters of flowing blood, such as diffusion, convection, flow and shear rates, are important as they determine the interaction of cells with vessel walls and prosthetic implants in the cardiovascular system. Most of the studies under flow conditions have been performed with platelets or other cells, and less attention has been paid to the effects that these parameters may cause on the adsorption of proteins. For this reason we studied how different shear rates affect the adsorption of human albumin, fibrinogen, total serum proteins, and complement factors 1q and 3c from human serum to silicon surfaces. The most relevant results indicate that during non-flow conditions the amount of adsorbed proteins is always lower than under flow. The different shear rates (225, 915, 1800 and 2700 s(-1)) all gave similar results, indicating that such a parameter is not very critical for single protein deposition. The differences in kinetics of complex protein solutions are conveniently highlighted by use of specific polyclonal antibodies. The difference between non-flow or low shear rate conditions and physiological flow conditions was enhanced for the complement cascade system.

Adsorption↗
PubMedDate not supplied

Isolation of the third component of complement and its derivative with anaphylatoxin-like activity from the plasma of the newt Cynops pyrrhogaster.

The third component of complement (C3) of a newt, Cynops pyrrhogaster, was purified using a fast protein liquid chromatography technique. The purified newt C3 consists of two polypeptide chains (the molecular masses of the alpha and beta-chains of C3 were 120,000 and 70,000, respectively) linked by disulfide bonds. The alpha-chain retained an internal thiolester bond that was cleaved with methylamine, and the N-terminal amino acid sequence of the alpha-chain was XVQLIDAKAGKAAKF. Digestion of newt C3 with trypsin yielded fragments that induced significant histamine release from newt peritoneal cells. These results indicate that newt C3 retains structural and functional properties shared with mammalian C3.

Amino Acid Sequence↗
PubMedDate not supplied

Opsonic complement system of the solitary ascidian, Halocynthia roretzi.

To elucidate the molecular architecture and function of the possibly primitive complement system of the solitary ascidian. Halochynthia roretzi, cDNA clones for the third component (C3) and mannose-binding lectin (MBL)-associated serine protease (MASP) were isolated from the hepatopancreas cDNA library. The deduced primary structure of ascidian C3 (AsC3) shows overall similarity to mammalian C3 including a typical thioester site. Two distinct ascidian MASPs, termed AsMASPa and AsMASPb, have the same domain structure as mammalian Clr/ Cls/MASP-1/MASP-2. Both of them show a closer similarity to mammalian MASP-1 than to mammalian Clr/Cls/ MASP-2. Ascidian body fluid contains an opsonic activity which enhances phagocytosis of yeast by ascidian blood cells, and an antibody against AsC3 inhibits this opsonic activity. These results indicate that the lectin-dependent, opsonic complement system was present prior to the emergence of the vertebrates and well ahead of the establishment of adaptive immunity.

Animals↗
PubMed1991

Intercellular adhesion molecule-1 (ICAM-1, CD 54) is associated with actin-filaments.

Intercellular adhesion molecule 1 (ICAM-1, CD 54) is a membrane associated glycoprotein involved in cell-cell interactions of the immune system. Detergent extraction of cultured human fibroblasts--stimulated with Interferon-gamma (IFN-gamma) for ICAM-1-expression--under conditions that stabilize actin in the filamentous (actin-F) form (NaF-buffer, phalloidine) resulted in greater retention of ICAM-1 in the detergent insoluble phase, containing the cytoskeletal matrix, compared to actin-F-destabilizing conditions (KCl-buffer). We further examined the in vitro ICAM-1 association with actin using immunoaffinity purified ICAM-1, prepared from either normal human tonsils or a spleen derived from a patient with Non-Hodgkin's lymphoma. ICAM-1 from both sources demonstrated binding to actin coated polystyrene surfaces. Our findings suggest that ICAM-1 interacts with actin-F and may use similar mechanisms described with other adhesion molecules for membrane-cytosol communication.

Actins↗
PubMed2000

Biodistribution of liposomes and C3 fragments associated with liposomes: evaluation of their relationship.

The biodistribution of liposomes with two different kind phospholipids (hydrogenated egg phosphatidylcholine and egg phosphatidylcholine) plus cholesterol (CHOL) were investigated after intravenous administration to rats. Elimination of liposomes from blood circulation was affected by the lipid composition. It appeared that the inclusion of CHOL in liposomes accelerates the rate of liposome uptake by liver, resulting in rapid elimination of liposomes. The amount of C3 fragments bound to liposomes was quantitatively determined to assess the contribution of the complement system to liposome accumulation into organs and liposome destabilization in vivo and in vitro. The amount of bound C3 fragments was directly proportional to CHOL content, and the amount was also proportional to the CLh, CLs as well as CLrel. This relationship suggests that the complement system is responsible for the elimination of liposomes from blood circulation, presumably as a consequence of opsonization by C3 fragments and assembly of membrane attack complex (MAC) onto liposomes. In addition, substitution of cholesteryl methyl ether into the liposome formulation for CHOL significantly diminished not only the binding of C3 fragments but also the CLh, CLs and CLrel, resulting in increased mean resident time (MRT) of the liposomes. This result suggests that the hydroxyl-group on CHOL is a binding site for C3 fragments on the liposomes and that CHOL in a liposome formulation promotes the accumulation of liposomes into the liver and spleen, probably due to their uptake by phagocytic cells, and impairs the stability of the liposomes in blood circulation, via a mechanism involving the complement system.

Animals↗
PubMed2001

Short term effect of atorvastatin and vitamin E on serum levels of C3, a sensitive marker of the risk of myocardial infarction in men.

C3 complement is produced in response to macrophage activation and is a reliable marker of the risk of myocardial infarction in men. This study was designed to ascertain whether the treatment with atorvastatin, a powerful cholesterol lowering drug, and/or vitamin E, a natural antioxidant, may induce a short term decrease in serum C3 in subjects with persistently elevated levels. From an initial random sample of 1100 men aged 55-64 years, 140 subjects with 3 consecutive C3 measurements in the high tertile (>1.19 g/l) were selected. Those with total cholesterol <5.56 mmol/l were double blindly randomized in groups 1 (placebo, N = 28, G1) and 2 (vitamin E 600 IU/day, N= 30, G2). The subjects with total cholesterol values >5.56 mmol/l were randomized in groups 3 (placebo, N= 30, G3), 4 (atorvastatin 10 mg/day, N = 27, G4) and 5 (atorvastatin 10 mg/day + vitamin E 600 IU/day, N = 25, G5). After 3 months C3 levels were substantially unchanged in the first 4 groups, while in G5 a very significant decrement occurred: -0.070 g/l (5.2%); 95% CI 0.043-0.098; p <0.0001. "Normal" levels of C3 (< 1.19 g/l) were reached by 28% of G5 subjects. In G2 and G5 vitamin E levels increased by 60 and 36%, while in G4 they decreased by 23% (p < 0.0001), paralleling cholesterol and triglyceride fall. In all groups a progressive decrease in HDL cholesterol occurred (-17%, p < 0.0001). In conclusion, treatment with atorvastatin plus vitamin E for three months can lower persistently elevated C3 levels.

Anticholesteremic Agents↗
PubMed1997

The comorbid association of migraine with osteoarthritis and hypertension: complement C3F and Berkson's bias.

Migraine is known to have a major genetic component and has been associated with a wide variety of comorbid disorders including arthritis and heart disease. Since migraine and some of its comorbid disorders involve inflammation, complement C3, a protein involved in acute inflammation, was selected for analysis as a candidate gene in an ongoing study of the genetic basis of migraine. Polymorphism frequencies for complement C3F (0.19) and C3S (0.81) in a sample of 137 unrelated migraineurs were found to be consistent with a control group as well as previous population studies, indicating that this common polymorphism has no association with migraine susceptibility. However, C3F positive individuals with migraine were found to have an increased incidence of osteoarthritis (Chi square = 10.06; p < 0.0008) and hypertension (Chi square = 5.18; p < 0.01). Therefore, the data in the present study indicate that certain migraine comorbidities that have been reported in the literature may result from Berkson's bias as opposed to a shared pathophysiological variation in the C3 gene.

Comorbidity↗
PubMed2001

Complement activation directly induced by Helicobacter pylori.

BACKGROUND AND AIMS: Helicobacter pylori is a frequent gram-negative colonizer of the human stomach. Its interaction with complement may be involved in the pathogenesis of chronic gastritis, and was mechanistically studied in vitro. METHODS: Four H. pylori strains, 2 cytotoxin-associated genes (cag)A+ and 2 cagA-, were isolated from infected patients. Bacteria or purified H. pylori lipopolysaccharides (LPSs) were incubated with nonimmune serum at 37 degrees C; the activation products C3b/iC3b/C3c (C3bc) and terminal complement complex (TCC) were then quantified by immunoassays. The serum sensitivity of 1 strain (L01, cagA+) was tested by counting the numbers of colony-forming units. RESULTS: All strains and LPSs generated large amounts of C3bc and TCC. Blocking of the classic complement pathway by the calcium chelator ethylene glycol tetraacetic acid (EGTA) markedly reduced the complement products, suggesting that H. pylori and its LPSs directly engage the classic activation pathway. H. pylori was shown to be serum sensitive, but 30% or more nonimmune serum was necessary to induce marked killing. After 5 minutes, swelled bacteria coated with C3bc and TCC were shown. CONCLUSIONS: H. pylori is complement sensitive and activates the classic pathway even in the absence of specific antibodies. Released cell wall constituents such as LPSs can activate complement and may explain why this bacterium induces gastric pathology without invading the mucosa.

Antibodies, Bacterial↗