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C Galanos

Publications and source records attributed to C Galanos.

At least 163 records · Page 9Linked to original sources
PubMed1979

[Lipid A antibody titers in patients after ureterosigmoidostomy (author's transl)].

Lipid A antibody titers were determined over a period of 6 months by passive hemolysis test in 10 patiens who underwent cystectomy and ureterosigmoidostomy. Preoperative the sera of all patients had no detectable anti lipid A activity. After 4 weeks 4 patients showed significant elevation of lipid A antibody titers. Only in these 4 patients the titers remained elevated up to six months. The significant elevation of lipid A antibody titers in these patients were caused by a non-obstructive infection of the kidneys. The serological determination of lipid A antibody titers appears to be an appropriate method for detecting pyelonephritis after ureterosigmoidostomy.

Aged↗
PubMed1978

Chemical structure and biological activities of lipid A's from various bacterial families.

The endotoxic principle of lipopolysaccharides (LPS) is localized in their lipid A component. Biological effects of LPS on, for instance, body temperature, blood pressure, and blood picture, are also induced by free lipid A. In contrast to the great variability of the 0-specific chains, the chemical structure of lipid A is much more constant. It is common for Salmonella and similar for other genera of the Enterobacteriaceae. Recently, a number of lipid A's have been recognized that exhibited distinct structural features compared with Enterobacteriaceae. These lipid A's were found to be also distinct with regard to some of their biological properties.

Carbohydrates↗
PubMed1978

Interaction of lipopolysaccharides and lipid A with complement in rats and its relation to endotoxicity.

Uniform salt forms of endotoxic lipopolysaccharides (LPS) and free lipid A showing distinct differences in their anticomplementary activity, as well as a nontoxic LPS, are used in a new approach of studying the role of complement in endotoxin shock. The use of these defined LPS forms led to the identification of two timely, distinct depressions in complement hemolytic activity after administration of endotoxin in rats. An early depression occurred within 10 min after injection, and a late one developed more gradually, with lowest values at 6 to 9 h. The early depression represents a direct interaction of LPS with complement. It was obtained by toxic and nontoxic preparations that exhibit a high molecular weight and anticomplementary activity in vitro. The early depression was not related to the toxic properties of the LPS. The late depression was obtained only with endotoxically active LPS in lethal and 100-fold-lower concentrations, regardless of their molecular weight and of their in vitro anticomplementary activity.

Animals↗
PubMed1977

B-cell activation by lipopolysaccharide. Distinct pathways for induction of mitosis and antibody production.

The role played by macrophages in two effects of lipopolysaccharide (LPS) on the immune system of the mouse-substitution for helper T cells and induction of B-cell mitosis-has been investigated. C3H/HeJ mice are unresponsive and do not produce (as other strains do) antibody to 2,4,6-trinitrophenol (TNP) conjugated with autologous mouse erythrocytes (MRBC-TNP) in the presence of LPS. We found that C3H/HeJ spleen cells produce antibody to MRBC-TNP when (a) LPS and macrophages from LPS-responsive C3HeB/FeJ mice or (b) tumor necrosis serum ([TNS] induced by LPS in responsive mice) are added. The mitotic response was not restored. The findings suggest that adjuvanticity and mitogenicity represent distinct pathways of B-cell activation by LPS, subject to different regulatory mechanisms.

Adjuvants, Immunologic↗
PubMed1977

[Occurence, significance and clinical consequences of lipid A antibody titers in patients with urinary tract infection (author's transl)].

Lipid A antibody titers were measured by the passive hemolysis test in 349 humans. In two out of 20 healthy adults and 16 out of 18 children with recurrent urinary tract infection (UTI) in the presence of anomalies anti-lipid A antibodies were present. In contrast, no titers were found in 23 newborn babies. In a group of 156 patients with acute UTI, 28% revealed positive titers, whereas in a group of 132 patients with recurrent UTI titers occurred in 81%. In a selected group of 132 patients with recurrent infections of the upper tract 59 (=96%) showed definite titers. There was no difference in the development of anti-lipid A antibodies between men and women and the height of the titers did not correlate with the clinical picture of the disease (acute or chronic). The combination of proteinuria and anti-lipid A antibodies indicates the presence of recurrent UTI or chronic pyelonephritis with about 90% accuracy. The titers are caused by immunogenically active lipid A in the body. Since lipid A has the ability to remain in the renal tissue for a long period of time and thereby to maintain the inflamatory response, long-term antimicrobial prophylaxis (six months) should be given to patients with a high risk of recurrent UTI.

Adolescent↗
PubMed1977

Lipid A antiserum-mediated protection against lipopolysaccharide- and lipid A-induced fever and skin necrosis.

The antiendotoxic activity of lipid A antiserum was studied in rabbits, using lipid A (lipopolysaccharide)-induced fever and skin necrosis as test systems. It was found that lipid A antiserum had no significant antipyretic effect when it was incubated with lipid A or injected intravenously before lipid A challenge. However, in animals that were pretreated (day 0) with a single dose of lipid A (lipopolysaccharide), a significant protective effect of passively transferred antiserum (day 1) to lipid A (lipopolysaccharide fever) (day 2) was observed. Also, the lipid A (lipopolysaccharide)-induced local shwartzman reaction could be prevented by lipid A antiserum. In the fever system, the degree of protection depended on the preparative and the challenge doses as well as on the amount of antiserum transferred. The fever protection mediated by lipid A antiserum seemed to be lipid A (lipopolysaccharide) specific with regard to both the preparative and the challenge injections. Lipid A specificity of the protective factor present in the antiserum was indicated by the fauggest that the factor might be identical with lipid A-specific immunoglobulin. The significance of the preparative injection is not understood at the present time. Iti is concluded, however, that in the fever protection system described, besides specific humoral factors, other factors, perhaps cellular, are involved.

Animals↗
PubMed1977

Biological activities of lipopolysaccharides and lipid A from Rhodospirillaceae.

The lipopolysaccharides and free lipid A from several strains of Rhodospirillaceae were assayed comparatively with those of Enterobacteriaceae in a number of biological tests. Free lipid A's from Rhodopseudomonas gelatinosa and Rhodospirillum tenue exhibited strong serological cross-reactions with each other and with free lipid A from Salmonella. Lipid A's from Rhodopseudomonas viridis and Rhodopseudomonas palustris, although cross-reacting with each other, did not do so with either the lipid A of R. gelatinosa or R. tenue or with that of Salmonella. The presence or absence of the above cross-reactions agreed with corresponding similarities or differences in the chemical structure of the lipid A preparations. The lipopolysaccharide of R. gelatinosa was highly toxic for adrenalectomized mice and pyrogenic for rabbits; however, it exhibited no anti-complementary activity. The activity of the R. tenue lipopolysaccharide was very low in both the lethality and pyrogenicity tests. Its corresponding free lipid A also exhibited low pyrogenic activity; however, its lethal toxicity for adrenalectomized mice was considerably higher than that of the intact parent lipopolysaccharide. Both intact lipopolysaccharide and, unexpectedly, the free lipid A exhibited no anti-complementary activity. The lipopolysaccharides of R. viridis and R. palustris were virtually nontoxic for mice and nonpyrogenic for rabbits. Both lipopolysaccharides were highly potent in their interaction with complement. They therefore represent the first example of nontoxic lipopolysaccharides exhibiting high anti-complementary activity.

Animals↗
PubMed1976

The role of the physical state of lipopolysaccharides in the interaction with complement. High molecular weight as prerequisite for the expression of anti-complementary activity.

Lipopolysaccharides interact with complement only when they are present in a state of high aggregation with a high apparent molecular weight. Lipopolysaccharides in uniform salt forms prepared by electrodialysis and neutralization with different bases exhibited distinct differences in their anticomplementary activity which correlated with differences in their sedimentation coefficients. Conversion of smooth (S) form lipopolysaccharides into the low-molecular-weight triethylamine form completely abolished their anti-complementary activity while conversion into the high-molecular-weight sodium form increased their activity. In contrast, a similar treatment of highly defective Re and Rd rough (R) form lipopolysaccharides had no effect on their ability to interact with complement. Both the triethylamine and sodium forms were strongly anti-complementary despite large differences in their molecular weight. This was found to be due to the property of R lipopolysaccharides to reaggregate into a large-molecular-weight form through absorption of Mg2+ and Ca2+ present in the guinea pig serum used as complement source. Defective lipopolysaccharides derived from the Ra and Rb classes showed only negligible anti-complementary activity which did not increase by conversion into salt forms with high molecular weight.

Amines↗
PubMed1976

Lipid A, the active part of bacterial endotoxins in inducing serum colony stimulating activity and proliferation of splenic granulocyte/macrophage progenitor cells.

An analysis of which component of lipopolysaccharides (LPS), the lipid or the polysaccharide (PS), is active in stimulating the murine granulopoietic system has been performed. LPS with different structures, isolated from different mutant strains of Salmonella and chemical degradation products of lipopolysaccharides have been used. Lipid A obtained by acid hydrolysys of the LPS and complexed to bovine serum albumin (BSA) (lipid A-BSA) was shown to be active in generating serum colony stimulating factor (CSF) and in increasing the splenic colony forming cells (CFC) levels, although it was less active than the parent LPS. The polysaccharide (PS) showed no significant activity at the concentrations used. LPS (glycolipids) from R mutants of Salmonella minnesota were active to the same extent as the LPS. The fact that even the most defective LPS from the R mutant R595 which contains lipid A and KDO only is a potent endotoxin, points unequivocally, to lipid A, as the active principle in stimulating the granulopoietic system.

Animals↗
PubMed1975

The lipoprotein of the outer membrane of Escherichia coli: a B-lymphocyte mitogen.

The lipoprotein of the outer membrane of Escherichia coli is a B-cell mitogen in mice. Polyclonal activation of B lymphocytes was measured by an increase in thymidine uptake, by the development of plaque-forming cells against densely coupled trinitrophenylated sheep red cells, and by selectively increased rates of synthesis and secretion of leucine-labeled IgM. Murein-free and muropeptides-containing lipoprotein are effective in B-cell activation, while free murein is inactive. Removal of ester-linked fatty acids from the amino-terminal end of the lipoprotein by alkaline hydrolysis abolishes the mitogenicity of the lipoprotein. B lymphocytes from high responder (C3H/Tif and BALB/c nu/nu) or from low responder (C3H/HeJ) mice to the mitogen lipopolysaccharide (LPS) both respond well to the lipoprotein. Anti-immunoglobulin antibodies inhibit the mitogenic stimulation of B cells by lipoprotein. A complex of structures including the Ig-receptor molecules, the LPS receptor, and the lipoprotein receptor appear involved in the regulation of mitogenic stimulation of B cells to proliferation and differentiation to IgM-secreting cells.

Animals↗
PubMed1975

Electrodialysis of lipopolysaccharides and their conversion to uniform salt forms.

Ions of low molecular weight like metal cations and basic amines are present in lipopolysaccharides regardless of the isolation procedure employed. They are present in salt form with the acidic groups of the molecule and, partly, bound by chelation. Electrodialysis which removed a large proportion of these basic materials led to acidic lipopolysaccharides often with reduced solubility. Electrodialyzed lopopolysaccharides could be rendered soluble by neutralizing with alkali or with a basic amine. Depending on the base employed for neutralization preparations were obtained which showed in water distinct differences in solubility, viscosity and opalescence. These differences were related to differences in the sedimentation coefficients of the various salt forms. Neutralization with triethylamine led in all cases to highly soluble preparations with low sedimentation coefficients, while, on the other hand, neutralization with Mg(OH)2 led in most cases to insoluble preparations. The acidic lipopolysaccharides obtained by electrodialysis deteriorate on storing in a freeze-dried form. On heating in distilled water autohydrolysis occurs and free lipid A is liberated. The lipid A which is so far known as a water-insoluble material showed increased solubility when prepared from electrodialyzed lipopolysaccharides.

Dialysis↗
PubMed1975

Experimental lipid A-induced nephritis in the dog.

The effect of radioactive lipid A, obtained from Escherichia coli, on the kidney of adult dogs and puppies was investigated. Injection of lipid A into the temporarily occluded renal pelvis of adult dogs caused abacterial interstitial nephritis in all animals tested. The intensity and duration of the kidney response coorelated well with the lipid A dose administered. Lipid A was demonstrated autoradiographically in the renal cortex, extra- and intracellularly. Radioactivity was still present after 10 weeks in 16 of 20 examined dogs. In the remaining four dogs the interstitial nephritis had subsided. Thirteen of 14 puppies in which the immunologic defense mechanisms had not yet developed showed no histologic reaction in the kidney after the same procedure as in the adult dogs. Lipid A appeared in the renal parenchyma through the blood stream rather than through the retrograde route. Lipid A antibody titers could be detected only in adult dogs, never in puppies. Lipid A apparently provoked an immunologic process in the kidney damaged by the operative manipulations, thus resulting in an abacterial interstitial nephritis. The possibility that chronic abacterial pyelonephritis can be induced clinically through lipid A and thus may have a pathogenesis similar to abacterial interstitial nephritis is discussed.

Animals↗
PubMed1975

Physical state and biological activity of lipopolysaccharides. Toxicity and immunogenicity of the lipid A component.

Bacterial lipopolysaccharides are negatively charged macromolecules due to the presence of phosphate, pyrophosphate and carboxyl groups. When isolated from bacteria, they are obtained in salt form with metal cations and basic amines. Removal of these ionically bound substances by electrodialysis leads to acidic lipopolysaccharides which on neutralizing with different bases, preparations are obtained which show distinct differences in their physico-chemical properties and in their biological activity. Soluble lipopolysaccharides interact with complement leading to loss of hemolytic activity. This property is embedded in the lipid A part of the molecule and is expressed only when the lipopolysaccharide is present in a favourable particle size. Nevertheless, a number of lipopolysaccharides exists, which, regardless of their particle size do not interact with complement. Lipid A is the part of the molecule responsible for endotoxicity. This was demonstrated by employing solubilized lipid A in complex form with BSA. Soluble lipid A/BSA complexes proved highly toxic for mice and pyrogenic in rabbits, and express many biological activities exhibited by intact lipopolysaccharides. Lipid A, when exposed on the bacterial cell-surface acts as a powerful immunogen, giving rise to the production of specific anti-lipid A antibodies that interact with the lipid A obtained from lipopolysaccharides that are otherwise distinct in their O-serological specificity. Anti-lipid A antibodies occur naturally in the serum of many animals and humans. The biological significance of anti-lipid A antibodies is discussed.

Antibodies, Bacterial↗
PubMed1973

The mitogenic effect of lipopolysaccharide on bone marrow-derived mouse lymphocytes. Lipid A as the mitogenic part of the molecule.

Lipopolysaccharides with different structure, isolated from different mutant strains of Escherichia coli and Salmonella bacteria, and chemical degradation products of these lipopolysaccharides have been employed to investigate which part of the lipopolysaccharide molecule exerts mitogenic effects on bone marrow-derived mouse lymphocytes. Within the structure of lipopolysaccharide consisting of lipid A, a core polysaccharide, and the O-polysaccharide antigen, lipid A was found to be the mitogenic part. The mitogenic effect of lipid A, consisting of phosphorylated glucosamine disaccharide units with ester- and amide-linked fatty acids, was lost after alkali treatment, which removes ester-linked fatty acids. Insertion of the lipid A portion of lipopolysaccharides into the lipid bilayer of the plasma membranes of bone marrow-derived lymphocytes is discussed as the initial mitogenic action.

Antibody Formation↗
PubMed1973

Pyrogenicity and immunogenicity of lipid A complexed with bovine serum albumin or human serum albumin.

The lipid A component of bacterial lipopolysaccharides (endotoxins), when complexed to bovine serum albumin (BSA) or human serum albumin (HSA), was shown to be a potent pyrogen. Furthermore, rabbits could be protected against endotoxin fever by immunization with both lipid A.BSA and lipid A.HSA complexes. The results presented in this paper show that lipid A is responsible for the pyrogenic activity of endotoxins and their ability to induce pyrogenic immunity.

Animals↗