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PubMed1978

Membrane phospholipid composition of Caulobacter crescentus.

The phospholipid composition of Caulobacter crescentus CB13 and CB15 was determined. The acidic phospholipids, phosphatidylglycerol and cardiolipin, comprise approximately 87% of the total phospholipids. Neither phosphatidylethanolamine nor its precursor phosphatidylserine was detected. The outer and inner membranes of C. crescentus CB13 were separated, and phospholipid analysis revealed heterogeneity with respect to the relative amounts of phosphatidylglycerol and cardiolipin in the two membranes. As has been shown to be the case for other bacterial membranes, the concentration of cardiolipin increases and phosphatidylglycerol decreases as cell cultures enter stationary phase.

Bacteria↗
PubMed1985

Cone-shaped lipids increase the susceptibility of phospholipids in bilayers to the action of phospholipases.

Addition of cardiolipin or diacylglycerol to dispersions of phosphatidylcholine greatly increased hydrolysis by snake venom or pancreatic phospholipase A2, as well as by a microbial phospholipase. Monogalactosyl diglyceride which, like cardiolipin and diacylglycerol, will form nonbilayer hexagonal II structures also caused an increase in the breakdown of phosphatidylcholine. Addition of digalactosyl diglyceride, a bilayer lipid from the same source, had a much smaller effect on the three phospholipases, indicating that stimulation by the nonbilayer lipids was not due to their fatty acid compositions. Stimulation of the microbial phospholipase by cardiolipin did not require the presence of calcium, leading to the conclusion that the formation of nonbilayer structures was not necessary. The results suggest that cone-shaped lipids increase the accessibility of lipids in bilayers to phospholipases by decreasing the packing of the polar head groups.

Animals↗
PubMed2003

Sulfatides: targets for anti-phospholipid antibodies.

BACKGROUND: Sulfatides are sulfated glycosphingolipids expressed on the surface of erythrocytes, leukocytes, and platelets. Sulfatides interact with several cell adhesion molecules involved in hemostasis. Beta2-glycoprotein I is an anionic phospholipid-binding plasma protein, and the phospholipid-bound form is the target for most anti-phospholipid antibodies that are associated with recurrent thrombosis, miscarriages, and neurological symptoms. In this study, we examined whether beta2-glycoprotein I forms a complex with sulfatides and thereby becomes a target for anti-phospholipid antibodies. METHODS AND RESULTS: Beta2-glycoprotein I binds to surface-bound sulfatides but not to other glycolipids, such as ceramide, cerebrosides, sphingomyelin, or ganglioside. At a sulfatide coating density of 1 microg/well, beta2-glycoprotein I reaches half-maximal binding at 2.5 microg/mL, and the binding is saturated at 10 microg/mL. The binding of beta2-glycoprotein I also depends on the coating density of sulfatides in the well. At a constant beta2-glycoprotein I concentration of 5 microg/mL, maximal binding of beta2-glycoprotein I is observed at a coating density of 1 mug/well. The serum from 14 patients with anti-cardiolipin antibodies, a subset of anti-phospholipid antibodies, bound to sulfatide-bound beta2-glycoprotein I and previous absorption on cardiolipin-coated surfaces decreased the immunoreactivity toward sulfatide-beta2-glycoprotein I complex by >50% in 12 of 14 patients. Furthermore, immunoaffinity-purified anti-cardiolipin antibodies from 4 of 5 patients reacted with sulfatide-bound beta2-glycoprotein I. CONCLUSIONS: These results show that not only anionic phospholipids, as commonly known, but also sulfatides are targets for most anti-phospholipid antibodies. We therefore postulate that interactions of these antibodies with sulfatides may contribute to some of the clinical symptoms of the anti-phospholipid antibody syndrome.

Antibodies, Anticardiolipin↗
PubMed1999

Involvement of Arg-328, Arg-334 and Arg-342 of DnaA protein in the functional interaction with acidic phospholipids.

We reported previously that three basic amino acids (Arg-360, Arg-364 and Lys-372) of DnaA protein are essential for its functional interaction with cardiolipin. In this study, we examined the effect of mutation of some basic amino acids in a potential amphipathic helix (from Lys-327 to Ile-345) of DnaA protein on this interaction. ATP binding to the mutant DnaA protein, in which Arg-328, Arg-334 and Arg-342 were changed to acidic amino acids, was less inhibited by cardiolipin than that of the wild-type protein, as was the case for mutant DnaA protein with mutations of Arg-360, Arg-364 and Lys-372. A mutant DnaA protein with mutations of all six basic amino acids showed the most resistance to the inhibition of ATP binding by cardiolipin. These results suggest that Arg-328, Arg-334 and Arg-342, like Arg-360, Arg-364 and Lys-372, are also involved in the functional interaction between DnaA protein and acidic phospholipids.

Adenosine Diphosphate↗
PubMed2001

[Effect of TFX preparation on the course of pregnancy in rabbits with experimental antiphospholipid syndrome].

Recurrent thrombo-embolic episodes and pregnancy loss, thrombocytopenia and the presence of antiphospholipid antibodies, first described in 1983 by Hughes and defined by Harris in 1987, are characteristic of the primary antiphospholipid syndrome (APS). APS is the cause of obstetrical problems in the form of recurrent miscarriages, intrauterine fetal death or growth retardation, and EPH gestosis. Clinical symptoms described above are probably mediated by antiphospholipid antibodies which interact with endothelial and trophoblastic cells, blood platelets, embryonic tissue cells, as well as with coagulation factors and proteins involved in the coagulation cascade or in antibody binding. Management of APS includes antiaggregation, anticoagulation, immunosuppression, and intravenous administration of gamma globulins. Successful treatment is not always the case and search for more efficient therapies continues. The importance of animal experiments led to the design at the Department of Pathology of Pregnancy and Labour of an APS model in pregnant and nonpregnant rabbits. As Turowski et al. have confirmed the immunomodulating action of TFX in rabbits, it seemed justified to examine the properties of this preparation in pregnant rabbits with experimentally induced APS. The material consisted of 30 pregnant New Zealand rabbits, divided into the following groups: I--10 pregnant rabbits (and 63 fetuses) treated intradermally twice weekly since the 10th day of pregnancy with cardiolipin together with adjuvant; I-K--5 pregnant rabbits (and 17 fetuses) treated with cardiolipin and adjuvant in the same manner as group I and additionally with intramuscular injections of 0.9% NaCl on the 20th, 21st, and 22nd day; I-T--10 pregnant rabbits (and 66 fetuses) treated with cardiolipin with adjuvant in the same manner as group I and additionally with intramuscular injections of 10 mg/day of TFX (Jelfa, Poland) on the 20th, 21st, and 22nd day of pregnancy; K--5 pregnant rabbits (and 27 fetuses) treated with injections of 0.9% NaCl twice weekly. Blood samples for laboratory analysis were collected by cardiac puncture before immunization (sample I) and on the day of caesarean section (sample II). Platelet counts and APTT tests were done. Numbers of live and dead newborns, resorbed fetuses, body mass, newborn viability and survival rates were recorded. TFX administered to pregnant rabbits with experimentally induced antiphospholipid syndrome increased the number of live newborns, reduced the incidence of fetal resorption, increased the viability and survival rate of newborn rabbits. The beneficial effect of TFX on APTT and platelet count was revealed, such that these parameters remained within the normal range despite immunization. Morphological changes observed in the placenta were not specific.

Animals↗
PubMed1976

The salt-resistance mechanism of Staphylococcus aureus examined by salt-sensitive mutants.

Two NaCl-sensitive mutants of S. aureus 209P (S-16 and S-23) were isolated after treatment of the parental strain with N-methyl-N'-nitro-N-nitrosoguanidine. Examination of the lipid components revealed that S-16 contained no cardiolipin and that S-23 contained only a small amount of cardiolipin. An increase of cardiolipin was indispensable for S. aureus proliferation in high NaCl medium.

Cardiolipins↗
PubMed1992

Anticardiolipin antibodies in NZW x BXSB F1 mice. A model of antiphospholipid syndrome.

NZW x BXSB F1 (W/B F1) male mice develop systemic lupus-like disease, and several autoantibodies, circulating immune complexes, and lupus nephritis become apparent. The abnormally high incidence of degenerative coronary vascular disease with myocardial infarction and thrombocytopenia due to the presence of both platelet-associated antibodies and circulating antiplatelet antibodies in this animal has been reported. We found that W/B F1 male mice produced autoantibodies against cardiolipin (aCL) and that the titer of aCL increases with age. aCL from W/B F1 male mice were mainly IgG and binding activity to cardiolipin was aCL-cofactor (beta 2-glycoprotein I (beta 2-GPI)) dependent. We developed monoclonal aCL from these animals and examined specificity of the autoantibodies. All the mAb used reacted with the negatively charged phospholipids, cardiolipin, phosphatidylserine, and phosphatidylinositol, and some reacted with platelets and DNA. The addition of human or mouse beta 2-GPI enhanced the titer for monoclonal aCL from the W/B F1 mice. From the results of competitive inhibition enzyme immunoassay with monoclonal aCL and purified beta 2-GPI, aCL from the W/B F1 mice recognized the complex of CL and beta 2-GPI. The W/B F1 male mouse may be an appropriate model for use in studies on the pathologic significance of aCL in patients with antiphospholipid syndrome.

Animals↗
PubMed1978

Identification of lipids associated with the ability of tumor cells to resist humoral immune attack.

Certain metabolic inhibitors or chemotherapeutic agents that increase the susceptibility of line-1 or line-10 guinea pig hepatoma cells to humoral immune attack were studied for their effects on the ability of the cells to synthesize lipids. A direct correlation was found between the drug-induced increase in sensitivity to antibody-C mediated killing and the inhibition of the ability of the cells to incorporate acetate, glycerol, and fatty acids into complex cellular lipids. Drug-treated cells recultured in drug-free medium regained their resistance to antibody-C mediated killing; these cells recovered their ability for complex lipid synthesis at this time. Thin layer chromatography of CHCl3:CH3OH lipid extracts from these cells indicated that the drug-induced increase in susceptibility to humoral immune attack correlated with the inhibition of acetate, glycerol, and fatty acid incorporation into cardiolipin and triglyceride in line-10 cells and the inhibition of incorporation of these compounds into cardiolipin alone in line-1 cells. No direct correlation was found between the sensitivity of the cells to humoral immune attack and the ability of the cells to incorporate precursors of lipid synthesis into other lipid moieties (sphyngomyelin, phosphatidyl serine, phosphatidyl choline, phosphatidyl glycerol, or cholesterol esters). The synthesis of cardiolipin and triglycerides, therefore, appears to be associated with the mechanism whereby these tumor cells resist antibody-C mediated killing.

Acetates↗
PubMedDate not supplied

The pathophysiology of anti-phospholipid antibodies.

Anti-phospholipids represent a heterogeneous family of antibodies able to react with the negatively charged phosphodiester groups of phospholipids. It includes the antibodies directed against the cardiolipin moiety of the VDRL antigen, the antibodies reacting with the phospholipids of the prothrombin activator complex and the antibodies able to react with solid phase cardiolipin. Data are reported indicating that reagins share distinct characteristics in comparison to the autoimmune anti-cardiolipin antibodies (ACA). On the contrary anti-phospholipid antibodies responsible for lupus-like anticoagulant activity display a quite similar reactivity with ACA, even if a complete overlapping cannot be demonstrated. The relationships between ACA and anti-DNA antibodies are also reported. The biological and clinical significance of these crossreactivities are discussed.

Autoantibodies↗
PubMed1989

[Fundamental examination and the reference values of anticardiolipin antibodies].

We studied sera from 146 healthy individuals in a fundamental examination to obtain reference values for anticardiolipin antibodies by the enzyme-linked immunosorbent assay (ELISA). The good results were obtained in the evaluation of concentrations of pretreatment substances, cardiolipin antigen and serum samples, as well as in reproducibility and stability on the storage of the samples. However, there was interference by triglycerides, hemoglobin and birilubin. The O.D. values and positive values of IgG, IgA and IgM in healthy individuals were 0.105, 0.111, 0.173 and 4.1%, 2.7%, 2.7% respectively. Furthermore, the incidences of anticardiolipin antibodies in systemic lupus erythematosus, mixed connective tissue disease, progressive systemic sclerosis, Sjogren's syndrome, polymyositis/dermatomyositis, rheumatoid arthritis, unclassified connective tissue disease, polyartertis nodosa and idiopathic thrombocytopenic purpura were 48.0%, 40.0%, 50.0%, 21.4%, 26.3%, 29.4%, 40.0% and 25.0% respectively. Especially, the incidence of IgG antibody against cardiolipin was high. Detection of phospholipid cardiolipin antibodies using ELISA was considered to be a useful for clinical diagnosis and monitoring of patients with systemic lupus erythematosus and associated autoimmune disorders.

Autoimmune Diseases↗
PubMed1988

Occurrence of both hemolytic anemia and thrombocytopenic purpura (Evans' syndrome) in systemic lupus erythematosus. Relationship to antiphospholipid antibodies.

Ten of 12 patients with systemic lupus erythematosus (SLE) who had hemolytic anemia and thrombocytopenic purpura (Evans' syndrome) during their course had evidence of antiphospholipid antibodies either because they had a false positive VDRL test (8 patients), a prolonged partial thromboplastin time (5 patients), a lupus anticoagulant (3/4 patients), and/or anticardiolipin antibodies as determined by an ELISA method (7 patients). Antibodies to cardiolipin were found in very high levels (up to 38 standard deviations above the mean of normal controls) and were of both IgG and IgM isotypes. The 2 patients with SLE and Evans' syndrome who did not have evidence of antiphospholipid antibodies were studied at the onset of SLE which occurred with Evans' syndrome. Although cardiolipin is not a constituent of the cell wall of either platelets or erythrocytes, other phospholipids that cross react antigenically with cardiolipin are and can be exposed through cell damage. This could be a mechanism whereby hemolytic anemia and thrombocytopenia could occur in the same patient with SLE. Whether absorption of the antiphospholipid antibody during the acute episode of hemocytopenia could occur, and thus prevent its detection at such time, remains undetermined.

Adult↗
PubMed1987

Transphosphatidylation activity in Clostridium butyricum. Evidence for a secondary pathway by which membrane phospholipids may be synthesized and modified.

Membrane particles from Clostridium butyricum, incubated with Triton X-100 and 32P-labeled phosphatidylethanolamine, phosphatidylglycerol, or phosphatidylserine, resulted in the labeling of three phospholipids. These unknown phospholipids incorporated label from the phosphate and acyl chains of the substrate, but not from the head group. Two-dimensional TLC of the intact lipids and their deacylation products showed that these lipids were phosphatidic acid, cardiolipin, and the previously unreported phosphatidyltriton. The reaction involved the transfer of the phosphatidyl moiety of the substrate molecule in a phospholipase D-like manner. The reaction displayed sigmoidal kinetics, did not require divalent cations, possessed an acidic pH optimum, and was sensitive to thermal inactivation. Differences in thermal sensitivity and pH optimum indicated that a distinct enzyme activity may be involved in the formation of cardiolipin. A primary alcohol group was required on the acceptor molecule, which could be either amphipathic or water-soluble. Addition of exogenous unlabeled phosphatidylglycerol resulted in the increased formation of cardiolipin, with a concomitant decrease in the level of phosphatidyltriton formed. Labeled phosphatidylethanolamine, phosphatidylglycerol, or phosphatidylserine could be formed upon addition of their corresponding alcoholic head group to incubations containing a 32P-labeled phosphatidyl donor and Triton X-100. These results indicate that, in C. butyricum, enzymic steps exist that would allow remodeling of the membrane phospholipids, without requiring de novo biosynthesis.

Cardiolipins↗
PubMed1973

Effects of acidic phospholipids, nucleotides, and heparin on the activity of lipase from rat liver lysosomes.

Purification and characterization of endogenous lipid factors that stimulate rat liver lysosomal lipase has led to the identification of cardiolipin, phosphatidylserine, and phosphatidic acid as stimulators of this activity. Bovine heart cardiolipin (half-maximal stimulation at 1.5 x 10(-4) m) and bovine brain phosphatidylserine (half-maximal stimulation at 9.5 x 10(-4) m) were the most potent of the phospholipids from other sources tested. The major rate-enhancing effect of phosphatidylserine is expressed as a 35-fold increase in the apparent V(max) of the enzyme. The effect is produced by acid phospholipids specifically, since in no case was there greater than a twofold stimulation by synthetic detergents, zwitterionic phospholipids, taurocholic acid, or gum acacia. The observed degree of stimulation depends upon the detergent used to disperse tripalmitin substrate and the relative concentrations of factor and detergent in reaction mixtures. The concentration of phosphatidylserine to produce half-maximal stimulation is directly dependent upon the Triton X-100 concentration, but the effects of this detergent on cardiolipin stimulation are more complex. Enzyme activity is inhibited 50% by 1 mm nucleoside triphosphate and 2.5 mm ADP, 80% by 1 mm PP(i), 100% by 20 U/ml heparin and 0.25 mg/ml chondroitin sulfate, and 80% by 10 mm sulfate ion. Inhibition is partially prevented by phosphatidylserine.

Animals↗
PubMed1979

Ionophoretic activities of phospholipids on human platelets.

The effects of phospholipids on calcium uptake by human platelets were investigated utilizing 45CaCl2. Among the phospholipids tested, cardiolipin and phosphatidic acid exerted a significant increase of calcium uptake by platelets. Calcium uptake was dependent upon cardiolipin concentration and incubation time. These phospholipids enhanced platelet aggregation induced by ADP (2 microM) or epinephrine (0.5 microgram/ml). Cardiolipin caused the significant release of serotonin from platelets in the absence of externally added calcium in the medium. These results may suggest that phospholipids activate platelets through their ionophoretic activities.

Biological Transport↗
PubMed1974

Skeletal muscle lipids. 3. Changes in fatty acid composition of individual phosphoglycerides in man from fetal to middle age.

The fatty acids in cardiolipin, choline phosphoglyceride, ethanolamine phosphoglyceride, inositol phosphoglyceride, and serine phosphoglyceride in the human gastrocnemius muscle were studied for changes between early fetal age to middle age. In cardiolipin, choline phosphoglyceride, and ethanolamine phosphoglyceride, the relative total amount of the linoleic acid series increased considerably during the prenatal period and reached maximum values during the first year of life. In inositol phosphoglyceride and serine phosphoglyceride, only slight changes in the sum of fatty acids of the linoleic acid series were found. An increase in the concentration of fatty acids of the linolenic acid series was found in ethanolamine phosphoglyceride and serine phosphoglyceride, while only minor amounts of these fatty acids were present in choline phosphoglyceride and inositol phosphoglyceride and not at all in cardiolipin. During the period studied, the amount of plasmalogen in ethanolamine phosphoglyceride decreased slightly during the first year of life and then remained at 40%. The amount of plasmalogen increased in choline phosphoglyceride from 8% at the middle of the gestational period to 15% 1 yr after birth. The individual phospholipids were found to have characteristic fatty acid patterns.

Adolescent↗
PubMed1981

[Limitations of passive treponema haemagglutination test (TPHA) in the detection of early syphilis (author's transl)].

The sera from 80 patients with clinical signs of primary syphilis were subjected to fluorescent treponemal antibody absorption test (FTA-abs), TPHA test and cardiolipin reactions (Kline, VDRL, Kolmer). The superiority of the FTA-abs test in screening for early primary syphilis was confirmed, but the TPHA test was less sensitive: the sera of 14 patients were reactive in the FTA-abs test and cardiolipins reactions but not in the TPHA test. The TPHA test alone cannot be relied upon to detect early syphilis; when the FTA-abs test is not performed, it must always be combined with one of the cardiolipin reactions.

Cardiolipins↗
PubMedDate not supplied

[Comparative effect of polymyxin B on lipid bilayer membranes with different lipid composition].

The aim of the work was to characterize the role of negatively charged lipids (cardiolipin and lauric acid) in the increase of ionic permeability of the membrane under the action of polymyxin B. Cardiolipin or lauric acid were added into membrane-forming solution in concentration close to that in the membrane of bacterial cell. It resulted in modification of membranes by these lipids. The obtained membranes had a higher ionic permeability in the presence of polymyxin B. However the comparison of different effects can lead to the conclusion that free fatty acid are responsible for the major part of the effect. It is concluded that the character of damage of the bilayer by polymyxin is diverse: polymyxin B forms ionic canals with lauric acid, whereas there is unspecific destruction of BLM by the polymyxin interacting with cardiolipin.

Cardiolipins↗
PubMed1997

Monoclonal antiphosphatidylserine antibodies react directly with feline and murine central nervous system.

OBJECTIVE: Antiphospholipid antibodies (aPL), especially against phosphatidylserine and cardiolipin, are associated with a variety of neurological disorders. While it is believed aPL react with endothelial cells to cause cerebral thrombosis, it is not known to what degree aPL react with neural tissue nor which particular aPL specificities may be more relevant. We investigated direct aPL reactivity with the central nervous system (CNS) using 3 monoclonal IgM aPL that differentiate between cardiolipin and phosphatidylserine dependent antigens. METHODS: Brain and spinal cord from normal cat Felis domesticus and brain from CD-1 mice were reacted with aPL using indirect immunoperoxidase techniques. Monoclonal aPL were reacted with whole brain myelin by dot immunoblots. RESULTS: Monoclonal D11A4, reactive with cardiolipin and not phosphatidylserine (CL+/PS-), did not react with any portion of the tissue. Both monoclonal 3SB9b (CL-/PS+) and BA3B5C4 (CL+/PS+) reacted in feline and murine CNS. Both labeled myelinated fibers in grey and white matter of brain and spinal cord in an identical pattern with positive control antibody against myelin basic protein and reacted with whole human brain myelin by dot immunoblot. 3SB9b (CL-+PS+) additionally reacted with ependyma and epithelium of the choroid plexus. CONCLUSION: aPL, especially those reactive with phosphatidylserine dependent antigens, react directly with epitopes associated with myelin, brain ependyma, or choroid epithelium. Direct reactivity of aPL with nervous tissue may be relevant to neurological disorders.

Animals↗