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PubMed1956

Studies on the O antigen of Salmonella typhosa. V. Enhancement of antibody response to protein antigens by the purified lipopolysaccharide.

Quantitative studies have demonstrated that a purified lipopolysaccharide (endotoxin) derived from the O-901 strain of Salmonella typhosa markedly enhanced the antibody response of rabbits when given separately or in conjunction with protein antigens. The augmentation of antibody levels varied from 2- to 40-fold with the number of injections, the dosage of antigen and endotoxin, and the route of administration. This antibody-enhancing property was found to be common to a broad group of endotoxins from Gram-negative bacilli and was not restricted to the lipopolysaccharide derived from S. typhosa. Factors affecting this enhancement were investigated, and data are presented which indicate that host susceptibility to endotoxin is a prerequisite for elevation of antibody levels; the intact lipopolysaccharide, as isolated, might not be essential for this activity; and the rate of clearance of antigen from the circulation of rabbits was accelerated when endotoxin was given in conjunction with protein. The data obtained are discussed in relation to postulated mechanisms on the antibody-enhancing action of endotoxin.

Animals↗
PubMed1956

Elevation of properdin levels in mice following administration of bacterial lipopolysaccharides.

The administration of a single small dose of bacterial lipopolysaccharide produces in mice a considerable rise in properdin levels. This is accompanied by an early, transient, non-specific increase in resistance to certain bacterial infections. Bacterial lipopolysaccharides were shown to possess far greater activity than other substances previously studied in bringing about an elevation of properdin levels. After the injection of bacterial lipopolysaccharides, high molecular weight substances appear in the circulation, which interfere with the combination of properdin with zymosan and thus affect the assay of properdin. The administration of small amounts of bacterial lipopolysaccharides to mice at appropriate times before experimental infection "conditions" the mice so that they maintain normal or elevated properdin titers during the infectious process in contrast to control mice which show a progressive decline in properdin to low levels and death. The significance of this observation and its relationship to natural resistance to Gram-negative pathogens are considered.

Animals↗
PubMed1956

Increased resistance to infection and accompanying alteration in properidin levels following administration of bacterial lipopolysaccharides.

It has been shown that injection of lipopolysaccharides, derived from a variety of Gram-negative bacterial species, evokes in mice a rapidly developing rise in resistance to infection with Gram-negative pathogens. This is accompanied by an elevation in properdin titer, at times to levels 2 to 3 times the normal. The rate, magnitude, and duration of these responses are dependent on many factors, the most important of which are the quantity and timing of the lipopolysaccharide administered. The increased resistance to infection evoked in mice by lipopolysaccharides was effective against infections produced by endotoxin-bearing organisms-bacterial species highly susceptible in vitro to the bactericidal action of the properdin system. Properdin titers of mice prior to infection provide an incomplete picture of the subsequent reaction of the host to the infective agent. Following infection with Gram-negative organisms, properdin levels accurately reflect the bacteriologic course and outcome of the infection. Thus, in control animals, properdin titers progressively declined and the animals died, while in mice appropriately treated with lipopolysaccharide, properdin levels were either maintained in the normal range or increased, depending on the dose and time of administration of lipopolysaccharide; this was always accompanied by successful management of the infection. The complex nature of the alterations produced in the host by lipopolysaccharides is stressed. It is pointed out that the increase in the ability of the host to cope with Gram-negative infections may be the result of stimulation of other defense mechanisms, in addition to the properdin system.

Animals↗
PubMed1957

Studies on the capacity of some polysaccharides to elicit antibody formation in man.

Purified levan is antigenic in man and subcutaneous injection of 1 mg. leads to the production of precipitins and skin sensitivity. Apple amylopectin, maize glycogen, and synthetic polyglucose did not stimulate antibody production in small numbers of individuals injected. Quantitative precipitin studies carried out with several levan preparations employing human antilevan show variations in immunochemical behavior indicating structural differences among levans. Evidence that precipitins formed in response to levan injection are antilevan antibodies was obtained by analysis of specific precipitates formed in the region of antibody excess for ketosugar. Injection of levan giving rise to production of antilevan failed in one individual to give a non-specific anamnestic rise in either antidextran or antiblood group A precipitins. Laminarin, a neutral polysaccharide, was found to give precipitation with normal human sera.

Antibodies↗
PubMed1957

Strain differences in local hemorrhagic response (Shwartzman-like reaction) of mice to a single intradermal injection of bacterial polysaccharides.

A survey of inbred strains of mice was made to determine whether the phenomenon of dermal hemorrhagic necrosis, as described in rabbits by Shwartzman, could be elicited in mice by bacterial polysaccharide preparations of demonstrated activity in rabbits. The polysaccharide preparations used were obtained from cultures of S. marcescens, S. typhosa, Ps. aeruginosa, and H. pertussis. Ten of the strains tested were unreactive. Three strains of mice and one F(1) hybrid subline developed a hemorrhagic lesion at the site of injection of a single, relatively high intradermal dose of polysaccharide. Some increase in incidence of hemorrhagic lesions was obtained when the intradermal dose was followed in 24 hours by an intravenous injection. In the gross and microscopically, the skin lesion produced in mice resembled the Shwartzman reaction in rabbits. An adrenergic blocking agent, SY-28, and an anticoagulant drug, coumadin, both of which block the dermal Shwartzman reaction in rabbits, also blocked the hemorrhagic skin reaction in mice.

Animals↗
PubMed1957

Similarity of host responses elicited by polysaccharides of animal and plant origin and by bacterial endotoxins.

Ten polysaccharides, isolated from various animal and plant sources, were selected for comparison with 2 bacterial polysaccharides, typical of Gram-negative endotoxins. The tissue sources were: mouse (kidney, liver, lung, stomach, Sarcoma 37, and Carcinoma 241-6); rabbit skin and chick embryo skin; and tangerine and Bryonia root. The bacterial endotoxins were those of S. typhosa and Serr. marcescens. Their relative potency was determined in inducing the following host effects: fever, tolerance to pyrogenic action, leucocytic changes, the Shwartzman reaction, damage to Sarcoma 37, dermal hemorrhagic-necrosis by epinephrine, enhancement of antibody production, and lethality. Some of the polysaccharides were consistently active in all the host reactions studied; except for pyrogenic activity at high dosage, the other polysaccharides were consistently negative throughout. The mouse tissue polysaccharides elicited all the effects studied; in some instances their potency approached those of the bacterial polysaccharides. It is pointed out that elicitation of the above array of biological phenomena, hitherto considered characteristic of bacterial endotoxins, can be obtained with polysaccharides from animal and plant tissues.

Animals↗
PubMed1957

The properdin system and immunity. VII. Alterations in properdin levels and resistance to infection in mice following the administration of tissue polysaccharides.

High molecular weight polysaccharide complexes derived from normal and neoplastic mammalian tissues were found to combine with properdin and to inactivate C'3 in vitro. These polysaccharide preparations were also found to alter properdin levels and non-specific resistance to Gram-negative infection in mice. In these manifestations, the tissue polysaccharides bore a marked resemblance to bacterial lipopolysaccharides. Some implications of the interactions of tissue polysaccharides and properdin in certain disease states are considered.

Animals↗
PubMed1959

The effects of bacterial endotoxin on lipide metabolism. I. The responses of the serum lipides of rabbits to single and repeated injections of Shear's polysaccharide.

Single intravenous injections of Shear's polysaccharide in varying dosages invariably produced an elevation in the levels of the total serum lipides 24 hours after injection of endotoxin. The total serum cholesterol and lipide phosphorus were also affected, although they did not change with smaller doses of endotoxin and were rarely elevated to the same degree as were the total serum lipides. The degree of elevation of the serum lipides was apparently related to the amount of endotoxin injected up to a certain point, beyond which there was no further increase. There were two types of response to endotoxin by the serum lipides, a moderate increase and an uncontrolled increase. Higher dosages of endotoxin and fasting apparently increased the incidence of the latter response. No direct correlation could be made between serum lipide responses and histologic evidence typical of the generalized Shwartzman reaction following this regimen of endotoxin injection. The Shwartzman reaction did occur with greater frequency and with lower dosages of endotoxin in fasted animals. Animals given repeated injections of endotoxin showed an initial increase in serum lipides followed by a progressive decrease to normal levels as tolerance to the febrile action of endotoxin appeared. The febrile tolerance as well as the unresponsiveness of the serum lipides to endotoxin was abolished by thorium dioxide (thorotrast) in these animals. In similar experiments a "breakthrough" of lipide unresponsiveness to endotoxin was obtained by increasing the amount of endotoxin injected. Some of the implications of these results for the metabolic alterations produced by bacterial endotoxins are discussed.

Animals↗